Updated on 2021/12/22

写真a

 
ASANUMA Masato
 
Organization
Faculty of Medicine, Dentistry and Pharmaceutical Sciences Professor
Position
Professor
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Degree

  • Ph.D.(MSci.) ( 1992.3   Okayama University )

Research Interests

  • Neuropharmacology

  • Neurology

  • Neurochemistry

Research Areas

  • Life Science / Neurology

  • Life Science / Neuroscience-general

  • Life Science / Pathophysiologic neuroscience

Education

  • Okayama University   医学研究科   生理系神経化学

    1988.4 - 1992.3

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    Country: Japan

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  • Okayama University   医学部   医学科

    1982.4 - 1988.3

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    Country: Japan

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Research History

  • Faculty of Pharmaceutical Sciences, Tokushima University   Part-time lecturer

    2016.4

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  • Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences   Department of Medical Neurobiology   Professor

    2014.7

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  • National Center of Neurology and Psychiatry   Division of Drug Dependence, National Institute of Mental Health   Part-time researcher

    2007.4

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  • Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences   Department of Brain Science   Associate Professor

    2001.4 - 2014.6

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  • Okayama University Medical School   Department of Neuroscience, Institute of Molecular and Cellular Medicine   Associate Professor (as old post name)

    2000.10 - 2001.3

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  • NIH/NIDA/IRP, U.S.A.   Molecular Neuropsychiatry Section, Cellular Neuroscience Branch   Visiting Fellow

    1996.9 - 1998.8

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    Country:United States

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  • Okayama University Medical School   Department of Neuroscience, Institute of Molecular and Cellular Medicine   Research Assistant

    1995.5 - 2000.9

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  • Okayama University Medical School   Department of Neuroscience, Institute of Molecular and Cellular Medicine   Part-time lecturer

    1995.4

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  • Japan Foundation for Aging and Health   Research Resident

    1994.4 - 1995.3

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  • Okayama University Medical School   Department of Neuroscience, Institute of Molecular and Cellular Medicine   Postdoctoral Research Fellow (Senior Staff Associate)

    1992.4 - 1994.3

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Professional Memberships

  • The Japanese Society of Toxicology

    2017.2

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  • 日本毒性学会生体金属部会(メタルバイオサイエンス研究会)

    2015.2

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  • The Japanese Association of Anatomists

    2012.8

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  • Movement Disorder Society Japan (MDSJ)

    2009.8

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  • The Japanese Pharmacological Society

    2008.1

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  • International Society for Neurochemistry (ISN)

    2004.7

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  • The Japanese Society of Neuropsychopharmacology

    1999.4

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  • Society for Neuroscience (SFN)

    1997.2

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  • Japan Neuroscience Society

    1995.5

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  • Japan Neurological Society

    1989.11

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  • The Japanese Neurochemical Society

    1989.10

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  • The Pharmaceutical Society of Japan

    2017.10

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  • The Japanese Society of Nutrition and Dietetics

    2010.5 - 2012

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  • The Japanese Young Researcher's Society of Neurobehavioral Pharmacology

    2010.3

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  • International Brain Research Organization

    1995.5

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  • International Society of Cerebral Blood Flow and Metabolism

    1993.5 - 2014

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  • The Japan Epilepsy Society

    1992.11 - 2007

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  • The Japan Brain Science Society

    1990.7 - 2021.3

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  • Japan Geriatrics Society

    1990 - 1995

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  • Japanese Society of Cerebral Blood Flow and Metabolism

    1990 - 1995

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  • The Japanese Society of Internal Medicine

    1989.2

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  • 岡山脳研究セミナー

    1989

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Committee Memberships

  • Japan Neurological Society   Councilor  

    2021.5   

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    Committee type:Academic society

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  • Movement Disorder Society Japan (MDSJ)   Councilor  

    2020.7   

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  • 日本薬理学会   代議員  

    2018.10   

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  • The Japanese Society of Toxicology   Councilor  

    2017.7   

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  • 日本神経精神薬理学会   企画委員会委員  

    2017.4   

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  • 日本神経精神薬理学会   先端研究推進基盤構築タスクフォース委員  

    2017.4   

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  • 日本毒性学会生体金属部会(メタルバイオサイエンス研究会)   常任幹事  

    2015.2   

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    メタルバイオサイエンス研究会

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  • The Japanese Association of Anatomists   Councilor  

    2014.8   

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  • The Japanese Pharmacological Society   Councilor  

    2013.4   

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  • The Japan Brain Science Society   Councilor  

    2006.6 - 2021.3   

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    Committee type:Academic society

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  • The Japanese Society of Neuropsychopharmacology   Councilor  

    2005.1   

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    Committee type:Academic society

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  • 岡山脳研究セミナー   事務局長  

    2000   

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    Committee type:Academic society

    岡山脳研究セミナー

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  • The Japanese Neurochemical Society   Councilor  

    1999.9   

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Papers

  • Neuroprotective Effects of Anti-high Mobility Group Box-1 Monoclonal Antibody Against Methamphetamine-Induced Dopaminergic Neurotoxicity Reviewed

    Kaori Masai, Keita Kuroda, Nami Isooka, Ryo Kikuoka, Shinki Murakami, Sunao Kamimai, Dengli Wang, Keyue Liu, Ikuko Miyazaki, Masahiro Nishibori, Masato Asanuma

    Neurotoxicity Research   39 ( 5 )   1511 - 1523   2021.10

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    Authorship:Last author, Corresponding author   Publishing type:Research paper (scientific journal)   Publisher:Springer Science and Business Media LLC  

    DOI: 10.1007/s12640-021-00402-5

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    Other Link: https://link.springer.com/article/10.1007/s12640-021-00402-5/fulltext.html

  • Glial cells as possible targets of neuroprotection through neurotrophic and antioxidative molecules in the central and enteric nervous systems in Parkinson’s disease. Reviewed

    Nami Isooka, Ikuko Miyazaki, Masato Asanuma

    Acta Medica Okayama   75 ( 5 )   549 - 556   2021.10

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  • Influence of 5-HT2A receptor function on anxiety-like behavior induced by a combination treatment with doxorubicin and cyclophosphamide in rats. Reviewed International journal

    Hironori Tabuchi, Yoshihisa Kitamura, Soichiro Ushio, Shiho Kan, Yudai Wada, Yusuke Sumiyoshi, Yasuhisa Izushi, Ikuko Miyazaki, Masato Asanuma, Toshiaki Sendo

    Psychopharmacology   2021.9

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    Language:English   Publishing type:Research paper (scientific journal)  

    Anxiety-like behavior induced by a combination of doxorubicin and cyclophosphamide may be mediated by serotonin (5-HT)2A receptor hyperactivity. The anxiolytic effects of fluoxetine may be inhibited by this combination. The present study examined the mechanisms underlying anxiety-like behavior induced by the combination doxorubicin and cyclophosphamide in rats. Anxiety-like behavior was induced during a light-dark test by the doxorubicin and cyclophosphamide treatment (once a week for 2 weeks). 5-HT2A receptor and 5-HT2A receptor-mediated extracellular signal-related kinase (ERK)1/2 levels were measured using Western blotting. 5-HT reuptake activity in fluoxetine-treated rats was also examined using microdialysis. ( ±)-1-(2,5-Dimethoxy-4-iodophenyl)-2-aminopropane, a 5-HT2A receptor agonist, induced anxiety-like behavior. The fluoxetine treatment increased extracellular 5-HT concentrations in the hippocampus of vehicle- and doxorubicin and cyclophosphamide-treated rats. 5-HT transporter levels in the hippocampus were not affected by chemotherapy. The doxorubicin and cyclophosphamide treatment did not alter 5-HT2A receptor levels in the frontal cortex. However, chemotherapy increased 5-HT2A receptor-mediated ERK1/2 phosphorylation levels significantly more than the vehicle treatment. The present results suggest that anxiety-like behavior induced by the combination of doxorubicin and cyclophosphamide is mediated by 5-HT2A receptor hyperactivity without an increase in 5-HT2A receptor levels in rats.

    DOI: 10.1007/s00213-021-05979-5

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  • Glutathione and Related Molecules in Parkinsonism Invited Reviewed

    Masato Asanuma, Ikuko Miyazaki

    International Journal of Molecular Sciences   22 ( 16 )   8689   2021.8

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    Authorship:Lead author, Corresponding author   Publishing type:Research paper (scientific journal)   Publisher:MDPI AG  

    Glutathione (GSH) is the most abundant intrinsic antioxidant in the central nervous system, and its substrate cysteine readily becomes the oxidized dimeric cystine. Since neurons lack a cystine transport system, neuronal GSH synthesis depends on cystine uptake via the cystine/glutamate exchange transporter (xCT), GSH synthesis, and release in/from surrounding astrocytes. Transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2), a detoxifying master transcription factor, is expressed mainly in astrocytes and activates the gene expression of various phase II drug-metabolizing enzymes or antioxidants including GSH-related molecules and metallothionein by binding to the antioxidant response element (ARE) of these genes. Accumulating evidence has shown the involvement of dysfunction of antioxidative molecules including GSH and its related molecules in the pathogenesis of Parkinson’s disease (PD) or parkinsonian models. Furthermore, we found several agents targeting GSH synthesis in the astrocytes that protect nigrostriatal dopaminergic neuronal loss in PD models. In this article, the neuroprotective effects of supplementation and enhancement of GSH and its related molecules in PD pathology are reviewed, along with introducing new experimental findings, especially targeting of the xCT-GSH synthetic system and Nrf2–ARE pathway in astrocytes.

    DOI: 10.3390/ijms22168689

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  • Lactoferrin-like Immunoreactivity in Distinct Neuronal Populations in the Mouse Central Nervous System. Reviewed

    Shigeyoshi Shimaoka, Hitomi Hamaoka, Junji Inoue, Masato Asanuma, Ikuo Tooyama, Yoichi Kondo

    Acta Medica Okayama   75 ( 2 )   153 - 167   2021.4

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    Language:English   Publishing type:Research paper (scientific journal)  

    Lactoferrin (Lf) is an iron-binding glycoprotein mainly found in exocrine secretions and the secondary granules of neutrophils. In the central nervous system (CNS), expression of the Lf protein has been reported in the lesions of some neurodegenerative disorders such as Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis, as well as in the aged brain. Lf is primarily considered an iron chelator, protecting cells from potentially toxic iron or iron-requiring microorganisms. Other biological functions of Lf include immunomodulation and transcriptional regulation. However, the roles of Lf in the CNS have yet to be fully clarified. In this study, we raised an antiserum against mouse Lf and investigated the immunohistochemical localization of Lf-like immunoreactivity (Lf-LI) throughout the CNS of adult mice. Lf-LI was found in some neuronal populations throughout the CNS. Intense labeling was found in neurons in the olfactory systems, hypothalamic nuclei, entorhinal cortex, and a variety of brainstem nuclei. This study provides detailed information on the Lf-LI distribution in the CNS, and the findings should promote further understanding of both the physiological and pathological significance of Lf in the CNS.

    DOI: 10.18926/AMO/61894

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  • アストロサイトの亜鉛関連分子を標的としたパーキンソン病治療戦略

    宮崎育子, 浅沼幹人

    日本薬理学雑誌   156 ( 2 )   76 - 80   2021.2

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  • パーキンソン病での神経保護標的としてのアストロサイトの抗酸化分子

    浅沼幹人, 宮崎育子

    日本薬理学雑誌   156 ( 1 )   14 - 20   2021.1

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  • N-Acetylcysteine Attenuates the Anxiety-Like Behavior and Spatial Cognition Impairment Induced by Doxorubicin and Cyclophosphamide Combination Treatment in Rats Reviewed

    Yoshihisa Kitamura, Soichiro Ushio, Yusuke Sumiyoshi, Yudai Wada, Ikuko Miyazaki, Masato Asanuma, Toshiaki Sendo

    Pharmacology   106 ( 5-6 )   286 - 293   2021

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    Publishing type:Research paper (scientific journal)   Publisher:S. Karger AG  

    <b><i>Background:</i></b> Cancer patients can suffer from psychological and cognitive disorders after chemotherapy, which influence quality of life. <b><i>Objective:</i></b> Oxidative stress may contribute to the psychological and cognitive disorders induced in rats by chemotherapy. In the present study, we examined the effects of N-acetylcysteine, an anti-oxidant, on anxiety-like behavior and cognitive impairment in rats treated with a combination of doxorubicin and cyclophosphamide. <b><i>Methods:</i></b> Rats were intraperitoneally injected with doxorubicin and cyclophosphamide once a week for 2 weeks. The light-dark test and the novel location recognition test were used to assess anxiety-like behavior and spatial cognition, respectively. The rats’ hippocampal levels of glutathione (GSH) and glutathione disulfide (GSSG) were measured using a GSSG/GSH quantification kit. <b><i>Results:</i></b> Combined treatment with doxorubicin and cyclophosphamide produced anxiety-like behavior and cognitive impairment in rats. N-acetylcysteine reversed the anxiety-like behavior and inhibition of novel location recognition induced by the combination treatment. Furthermore, the combination of doxorubicin and cyclophosphamide significantly reduced the rats’ hippocampal GSH/GSSG ratios. N-acetylcysteine reversed the reduction in the GSH/GSSG ratio seen in the doxorubicin and cyclophosphamide-treated rats. <b><i>Conclusion:</i></b> These results suggest that N-acetylcysteine inhibits doxorubicin and cyclophosphamide-induced anxiety-like behavior and cognitive impairment by reducing oxidative stress in the hippocampus.

    DOI: 10.1159/000512117

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  • Neuron-Astrocyte Interactions in Parkinson’s Disease Invited Reviewed

    Ikuko Miyazaki, Masato Asanuma

    Cells   9 ( 12 )   2623   2020.12

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    Parkinson’s disease (PD) is the second most common neurodegenerative disease. PD patients exhibit motor symptoms such as akinesia/bradykinesia, tremor, rigidity, and postural instability due to a loss of nigrostriatal dopaminergic neurons. Although the pathogenesis in sporadic PD remains unknown, there is a consensus on the involvement of non-neuronal cells in the progression of PD pathology. Astrocytes are the most numerous glial cells in the central nervous system. Normally, astrocytes protect neurons by releasing neurotrophic factors, producing antioxidants, and disposing of neuronal waste products. However, in pathological situations, astrocytes are known to produce inflammatory cytokines. In addition, various studies have reported that astrocyte dysfunction also leads to neurodegeneration in PD. In this article, we summarize the interaction of astrocytes and dopaminergic neurons, review the pathogenic role of astrocytes in PD, and discuss therapeutic strategies for the prevention of dopaminergic neurodegeneration. This review highlights neuron-astrocyte interaction as a target for the development of disease-modifying drugs for PD in the future.

    DOI: 10.3390/cells9122623

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  • Mirtazapine exerts astrocyte-mediated dopaminergic neuroprotection Reviewed

    Ryo Kikuoka, Ikuko Miyazaki, Natsuki Kubota, Megumi Maeda, Daiki Kagawa, Masaaki Moriyama, Asuka Sato, Shinki Murakami, Yoshihisa Kitamura, Toshiaki Sendo, Masato Asanuma

    Scientific Reports   10 ( 1 )   20698   2020.12

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    <title>Abstract</title>Mirtazapine, a noradrenergic and specific serotonergic antidepressant (NaSSA), is known to activate serotonin (5-HT) 1A receptor. Our recent study demonstrated that stimulation of astrocytic 5-HT1A receptors promoted astrocyte proliferation and upregulated antioxidative property in astrocytes to protect dopaminergic neurons against oxidative stress. Here, we evaluated the neuroprotective effects of mirtazapine against dopaminergic neurodegeneration in models of Parkinson’s disease (PD). Mirtazapine administration attenuated the loss of dopaminergic neurons in the substantia nigra and increased the expression of the antioxidative molecule metallothionein (MT) in the striatal astrocytes of 6-hydroxydopamine (6-OHDA)-injected parkinsonian mice via 5-HT1A receptors. Mirtazapine protected dopaminergic neurons against 6-OHDA-induced neurotoxicity in mesencephalic neuron and striatal astrocyte cocultures, but not in enriched neuronal cultures. Mirtazapine-treated neuron-conditioned medium (Mir-NCM) induced astrocyte proliferation and upregulated MT expression via 5-HT1A receptors on astrocytes. Furthermore, treatment with medium from Mir-NCM-treated astrocytes protected dopaminergic neurons against 6-OHDA neurotoxicity, and these effects were attenuated by treatment with a MT-1/2-specific antibody or 5-HT1A antagonist. Our study suggests that mirtazapine could be an effective disease-modifying drug for PD and highlights that astrocytic 5-HT1A receptors may be a novel target for the treatment of PD.

    DOI: 10.1038/s41598-020-77652-4

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    Other Link: http://www.nature.com/articles/s41598-020-77652-4

  • The Rotenone Models Reproducing Central and Peripheral Features of Parkinson’s Disease Reviewed

    Ikuko Miyazaki, Masato Asanuma

    NeuroSci   1 ( 1 )   1 - 14   2020.8

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    Parkinson’s disease (PD) is a complex, multi-system, neurodegenerative disorder; PD patients exhibit motor symptoms (such as akinesia/bradykinesia, tremor, rigidity, and postural instability) due to a loss of nigrostriatal dopaminergic neurons, and non-motor symptoms such as hyposmia, autonomic disturbance, depression, and REM sleep behavior disorder (RBD), which precedes motor symptoms. Pathologically, α-synuclein deposition is observed in the central and peripheral nervous system of sporadic PD patients. To clarify the mechanism of neurodegeneration in PD and to develop treatment to slow or stop PD progression, there is a great need for experimental models which reproduce neurological features of PD. Animal models exposed to rotenone, a commonly used pesticide, have received most attention since Greenamyre and his colleagues reported that chronic exposure to rotenone could reproduce the anatomical, neurochemical, behavioral, and neuropathological features of PD. In addition, recent studies demonstrated that rotenone induced neuropathological change not only in the central nervous system but also in the peripheral nervous system in animals. In this article, we review rotenone models especially focused on reproducibility of central and peripheral multiple features of PD. This review also highlights utility of rotenone models for investigation of PD pathogenesis and development of disease-modifying drugs for PD in future.

    DOI: 10.3390/neurosci1010001

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  • The neurotoxicity of psychoactive phenethylamines “2C series” in cultured monoaminergic neuronal cell lines Reviewed

    Masato Asanuma, Ikuko Miyazaki, Masahiko Funada

    Forensic Toxicology   38 ( 2 )   394 - 408   2020.7

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    Authorship:Lead author, Corresponding author   Publishing type:Research paper (scientific journal)   Publisher:Springer Science and Business Media LLC  

    DOI: 10.1007/s11419-020-00527-w

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    Other Link: http://link.springer.com/article/10.1007/s11419-020-00527-w/fulltext.html

  • Cerebellar Blood Flow and Gene Expression in Crossed Cerebellar Diaschisis after Transient Middle Cerebral Artery Occlusion in Rats Reviewed

    Naoya Kidani, Tomohito Hishikawa, Masafumi Hiramatsu, Shingo Nishihiro, Kyohei Kin, Yu Takahashi, Satoshi Murai, Kenji Sugiu, Takao Yasuhara, Ikuko Miyazaki, Masato Asanuma, Isao Date

    International Journal of Molecular Sciences   21 ( 11 )   4137   2020.6

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    Crossed cerebellar diaschisis (CCD) is a state of hypoperfusion and hypometabolism in the contralesional cerebellar hemisphere caused by a supratentorial lesion, but its pathophysiology is not fully understood. We evaluated chronological changes in cerebellar blood flow (CbBF) and gene expressions in the cerebellum using a rat model of transient middle cerebral artery occlusion (MCAO). CbBF was analyzed at two and seven days after MCAO using single photon emission computed tomography (SPECT). DNA microarray analysis and western blotting of the cerebellar cortex were performed and apoptotic cells in the cerebellar cortex were stained. CbBF in the contralesional hemisphere was significantly decreased and this lateral imbalance recovered over one week. Gene set enrichment analysis revealed that a gene set for “oxidative phosphorylation” was significantly upregulated while fourteen other gene sets including “apoptosis”, “hypoxia” and “reactive oxygen species” showed a tendency toward upregulation in the contralesional cerebellum. MCAO upregulated the expressions of nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) in the contralesional cerebellar cortex. The number of apoptotic cells increased in the molecular layer of the contralesional cerebellum. Focal cerebral ischemia in our rat MCAO model caused CCD along with enhanced expression of genes related to oxidative stress and apoptosis.

    DOI: 10.3390/ijms21114137

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  • Chronic Systemic Exposure to Low-Dose Rotenone Induced Central and Peripheral Neuropathology and Motor Deficits in Mice: Reproducible Animal Model of Parkinson’s Disease Reviewed

    Ikuko Miyazaki, Nami Isooka, Fuminori Imafuku, Jin Sun, Ryo Kikuoka, Chieko Furukawa, Masato Asanuma

    International Journal of Molecular Sciences   21 ( 9 )   3254   2020.5

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    Epidemiological studies demonstrated that pesticide exposure, such as rotenone and paraquat, increases the risk of Parkinson’s disease (PD). Chronic systemic exposure to rotenone, a mitochondrial complex I inhibitor, could reproduce many features of PD. However, the adoption of the models is limiting because of variability in animal sensitivity and the inability of other investigators to consistently reproduce the PD neuropathology. In addition, most of rotenone models were produced in rats. Here, we tried to establish a high-reproducible rotenone model using C57BL/6J mice. The rotenone mouse model was produced by chronic systemic exposure to a low dose of rotenone (2.5 mg/kg/day) for 4 weeks by subcutaneous implantation of rotenone-filled osmotic mini pump. The rotenone-treated mice exhibited motor deficits assessed by open field, rotarod and cylinder test and gastrointestinal dysfunction. Rotenone treatment decreased the number of dopaminergic neuronal cells in the substantia nigra pars compacta (SNpc) and lesioned nerve terminal in the striatum. In addition, we observed significant reduction of cholinergic neurons in the dorsal motor nucleus of the vagus (DMV) and the intestinal myenteric plexus. Moreover, α-synuclein was accumulated in neuronal soma in the SNpc, DMV and intestinal myenteric plexus in rotenone-treated mice. These data suggest that the low-dose rotenone mouse model could reproduce behavioral and central and peripheral neurodegenerative features of PD and be a useful model for investigation of PD pathogenesis.

    DOI: 10.3390/ijms21093254

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  • Effects of maternal bisphenol A diglycidyl ether exposure during gestation and lactation on behavior and brain development of the offspring Reviewed

    Ikuko Miyazaki, Ryo Kikuoka, Nami Isooka, Mika Takeshima, Kanau Sonobe, Rei Arai, Hidemaru Funakoshi, Kyle E. Quin, Jonathan Smart, Kazumasa Zensho, Masato Asanuma

    Food and Chemical Toxicology   138   111235   2020.4

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    DOI: 10.1016/j.fct.2020.111235

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  • Dopaminergic neuroprotective effects of rotigotine via 5-HT1A receptors: Possibly involvement of metallothionein expression in astrocytes Reviewed

    Nami Isooka, Ikuko Miyazaki, Ryo Kikuoka, Kouichi Wada, Erika Nakayama, Kotaro Shin, Daichi Yamamoto, Yoshihisa Kitamura, Masato Asanuma

    Neurochemistry International   132   104608   2020.1

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    Authorship:Last author, Corresponding author   Publishing type:Research paper (scientific journal)   Publisher:Elsevier BV  

    DOI: 10.1016/j.neuint.2019.104608

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  • Attenuation of Macrophage Migration Inhibitory Factor-Stimulated Signaling via S-Nitrosylation Reviewed

    Kengo Nakahara, Kana Fujikawa, Hideki Hiraoka, Ikuko Miyazaki, Masato Asanuma, Akihiro Ito, Nobumasa Takasugi, Takashi Uehara

    Biological and Pharmaceutical Bulletin   42 ( 6 )   1044 - 1047   2019.6

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    Publishing type:Research paper (scientific journal)   Publisher:Pharmaceutical Society of Japan  

    DOI: 10.1248/bpb.b19-00025

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  • Effects of Enteric Environmental Modification by Coffee Components on Neurodegeneration in Rotenone-Treated Mice Reviewed

    Ikuko Miyazaki, Nami Isooka, Kouichi Wada, Ryo Kikuoka, Yoshihisa Kitamura, Masato Asanuma

    Cells   8 ( 3 )   221   2019.3

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    Authorship:Last author   Publishing type:Research paper (scientific journal)   Publisher:MDPI AG  

    Epidemiological studies have shown that coffee consumption decreases the risk of Parkinson’s disease (PD). Caffeic acid (CA) and chlorogenic acid (CGA) are coffee components that have antioxidative properties. Rotenone, a mitochondrial complex I inhibitor, has been used to develop parkinsonian models, because the toxin induces PD-like pathology. Here, we examined the neuroprotective effects of CA and CGA against the rotenone-induced degeneration of central dopaminergic and peripheral enteric neurons. Male C57BL/6J mice were chronically administered rotenone (2.5 mg/kg/day), subcutaneously for four weeks. The animals were orally administered CA or CGA daily for 1 week before rotenone exposure and during the four weeks of rotenone treatment. Administrations of CA or CGA prevented rotenone-induced neurodegeneration of both nigral dopaminergic and intestinal enteric neurons. CA and CGA upregulated the antioxidative molecules, metallothionein (MT)-1,2, in striatal astrocytes of rotenone-injected mice. Primary cultured mesencephalic or enteric cells were pretreated with CA or CGA for 24 h, and then further co-treated with a low dose of rotenone (1–5 nM) for 48 h. The neuroprotective effects and MT upregulation induced by CA and CGA in vivo were reproduced in cultured cells. Our data indicated that intake of coffee components, CA and CGA, enhanced the antioxidative properties of glial cells and prevents rotenone-induced neurodegeneration in both the brain and myenteric plexus.

    DOI: 10.3390/cells8030221

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  • Region-Specific Neuroprotective Features of Astrocytes against Oxidative Stress Induced by 6-Hydroxydopamine Reviewed

    Masato Asanuma, Nao Okumura-Torigoe, Ikuko Miyazaki, Shinki Murakami, Yoshihisa Kitamura, Toshiaki Sendo

    International Journal of Molecular Sciences   20 ( 3 )   598   2019.1

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    Authorship:Lead author, Corresponding author   Publishing type:Research paper (scientific journal)   Publisher:MDPI AG  

    In previous studies, we found regional differences in the induction of antioxidative molecules in astrocytes against oxidative stress, postulating that region-specific features of astrocytes lead region-specific vulnerability of neurons. We examined region-specific astrocytic features against dopaminergic neurotoxin 6-hydroxydopamine (6-OHDA) as an oxidative stress using co-culture of mesencephalic neurons and mesencephalic or striatal astrocytes in the present study. The 6-OHDA-induced reduction of mesencephalic dopamine neurons was inhibited by co-culturing with astrocytes. The co-culture of midbrain neurons with striatal astrocytes was more resistant to 6-OHDA than that with mesencephalic astrocytes. Furthermore, glia conditioned medium from 6-OHDA-treated striatal astrocytes showed a greater protective effect on the 6-OHDA-induced neurotoxicity and oxidative stress than that from mesencephalic astrocytes. The cDNA microarray analysis showed that the number of altered genes in both mesencephalic and striatal astrocytes was fewer than that changed in either astrocyte. The 6-OHDA treatment, apparently up-regulated expressions of Nrf2 and some anti-oxidative or Nrf2-regulating phase II, III detoxifying molecules related to glutathione synthesis and export in the striatal astrocytes but not mesencephalic astrocytes. There is a profound regional difference of gene expression in astrocytes induced by 6-OHDA. These results suggest that protective features of astrocytes against oxidative stress are more prominent in striatal astrocytes, possibly by secreting humoral factors in striatal astrocytes.

    DOI: 10.3390/ijms20030598

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  • Involvement of 5-HT2A receptor hyperfunction in the anxiety-like behavior induced by doxorubicin and cyclophosphamide combination treatment in rats Reviewed

    Yuka Nakamura, Yoshihisa Kitamura, Yusuke Sumiyoshi, Nanami Naito, Shiho Kan, Soichiro Ushio, Ikuko Miyazaki, Masato Asanuma, Toshiaki Sendo

    Journal of Pharmacological Sciences   138 ( 3 )   192 - 197   2018.11

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    Publishing type:Research paper (scientific journal)   Publisher:Elsevier BV  

    DOI: 10.1016/j.jphs.2018.10.001

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  • Application of Single Prolonged Stress Induces Post-traumatic Stress Disorder-like Characteristics in Mice. Reviewed

    Ken-Ichi Tanaka, Takao Yagi, Takeshi Nanba, Masato Asanuma

    Acta Medica Okayama   72 ( 5 )   479 - 485   2018.10

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    © 2018, by Okayama University Medical School. We tried to clarify the applicability of a single prolonged stress (SPS) protocol as post-traumatic stress disorder (PTSD) model in mice. To investigate PTSD pathophysiology, we conducted hypothalamo-pituitary-adrenal (HPA) negative feedback testing at 1, 4, 8 and 12 weeks after the SPS by administrating a dexamethasone (DEX) suppression test. The SPS induced over-suppression of the HPA system by DEX treatment at 8 and 12 weeks. To investigate PTSD-like behavioral characteristics, we subjected mice to testing in a light/dark box (to assess anxiety), a Y-maze (working memory), a cliff avoidance (visual cognition), and an open field (locomotor activity) at 1, 4, 8 and 12 weeks after the SPS. In the light/dark box test, the SPS-applied mice spent significantly less time in the light box at 8 or 12 weeks. In the cliff avoidance test, the SPS-applied mice spent significantly less time in the open area at 1 week. However, in both the Y-maze test and the open field test, SPS-applied mice tended toward slight decreases in a time-dependent manner until 12 weeks. Therefore, SPS-applied mice may thus be useful for assessing characteristics relevant to PTSD that coincide with changes in the HPA axis.

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  • Neuroprotective effect of fermented papaya preparation by activation of Nrf2 pathway in astrocytes Reviewed

    Shinki Murakami, Ikuko Miyazaki, Masato Asanuma

    Nutritional Neuroscience   21 ( 3 )   176 - 184   2018.3

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    DOI: 10.1080/1028415x.2016.1253171

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  • Influence of nicotine on doxorubicin and cyclophosphamide combination treatment-induced spatial cognitive impairment and anxiety-like behavior in rats Reviewed

    Yoshihisa Kitamura, Erika Kanemoto, Misaki Sugimoto, Ayumi Machida, Yuka Nakamura, Nanami Naito, Hirotaka Kanzaki, Ikuko Miyazaki, Masato Asanuma, Toshiaki Sendo

    Naunyn-Schmiedeberg's Archives of Pharmacology   390 ( 4 )   369 - 378   2017.4

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    DOI: 10.1007/s00210-016-1338-z

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  • Therapeutic strategy of targeting astrocytes for neuroprotection in parkinson’s disease Reviewed

    Ikuko Miyazaki, Masato Asanuma

    Current Pharmaceutical Design   23 ( 33 )   4936 - 4947   2017

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    Parkinson’s disease (PD) is one of common neurodegenerative diseases, which shows motor symptoms including tremor, bradykinesia, rigidity and postural instability. It also involves non-motor symptoms such as cognitive impairment, mental manifestation, autonomic disorder and sensory disturbance. Although treatments to improve the motor disability in PD are being assessed at present, the main challenge remains that is the development of neuroprotective or disease-modifying treatments. Therefore, it is desirable to find approaches that can inhibit the progression of dopaminergic neurodegeneration. Astrocytes are known to play an important role in the maintenance of the neuronal environment and exert neuroprotective effects. Additionally, astrocyte dysfunction increases the susceptibility of neurons to cytotoxicity. We have demonstrated neuroprotective approaches in parkinsonian models in various studies targeting astrocytes. In this article, we summarize the neuroprotective function of astrocytes in the brain, involvement of astrocyte dysfunction in neurodegeneration, and experimental approaches to dopaminergic neuroprotection. We review findings reported in several papers including our own studies. We also address target molecules and pivotal pathways in astrocytes for dopaminergic neuroprotection. The review discusses new promising therapeutic strategies to prevent dopaminergic neurodegeneration in PD.

    DOI: 10.2174/1381612823666170710163731

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  • Identification of transcription factors activated by methylmercury in mouse brain Reviewed

    Min-Soek Kim, Tsutomu Takahashi, Jin-Yong Lee, Nobuhiko Miura, Masato Asanuma, Gi-Wook Hwang, Akira Naganuma

    Fundamental Toxicological Sciences   4 ( 1 )   37 - 39   2017

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    DOI: 10.2131/fts.4.37

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  • Effect of alteration of glutathione content on cell viability in a-synuclein-transfected SH-SY5Y cells. Reviewed

    Tanaka, K, Sonoda, K, Asanuma, M

    Advances in Parkinson's Disease   6   93 - 100   2017

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    DOI: 10.4236/apd.2017.63010

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  • 3-O-Methyldopa inhibits astrocyte-mediated dopaminergic neuroprotective effects of l-DOPA Reviewed

    Masato Asanuma, Ikuko Miyazaki

    BMC Neuroscience   17 ( 1 )   52   2016.12

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    DOI: 10.1186/s12868-016-0289-0

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  • L-Theanine protects against excess dopamine-induced neurotoxicity in the presence of astrocytes Reviewed

    Mika Takeshima, Ikuko Miyazaki, Shinki Murakami, Taizo Kita, Masato Asanuma

    Journal of Clinical Biochemistry and Nutrition   59 ( 2 )   93 - 99   2016.9

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    DOI: 10.3164/jcbn.16-15

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  • In vitro quantitative determination of the concentration of the polymerization agent methyl 2-benzoylbenzoate in intravenous injection solution and the cytotoxic effects of the chemical on normal human peripheral blood mononuclear cells Reviewed

    Chiaki Tsuboi, Yoichi Kawasaki, Kei Yoshitome, Kenta Yagi, Taro Miura, Satoru Esumi, Ikuko Miyazaki, Masato Asanuma, Yoshihisa Kitamura, Toshiaki Sendo

    Environmental Science and Pollution Research   23 ( 10 )   10262 - 10269   2016.5

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    DOI: 10.1007/s11356-016-6332-y

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  • Neuroprotective effects of levetiracetam target xCT in astrocytes in parkinsonian mice Reviewed

    Ikuko Miyazaki, Shinki Murakami, Nao Torigoe, Yoshihisa Kitamura, Masato Asanuma

    Journal of Neurochemistry   136 ( 1 )   194 - 204   2016.1

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    DOI: 10.1111/jnc.13405

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  • Anti-high mobility group box 1 antibody exerts neuroprotection in a rat model of Parkinson's disease Reviewed

    Tatsuya Sasaki, Keyue Liu, Takashi Agari, Takao Yasuhara, Jun Morimoto, Mihoko Okazaki, Hayato Takeuchi, Atsuhiko Toyoshima, Susumu Sasada, Aiko Shinko, Akihiko Kondo, Masahiro Kameda, Ikuko Miyazaki, Masato Asanuma, Cesario V. Borlongan, Masahiro Nishibori, Isao Date

    Experimental Neurology   275   220 - 231   2016.1

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    DOI: 10.1016/j.expneurol.2015.11.003

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  • Serotonin 1A Receptors on Astrocytes as a Potential Target for the Treatment of Parkinson's Disease Reviewed

    Ikuko Miyazaki, Masato Asanuma

    Current Medicinal Chemistry   23 ( 7 )   686 - 700   2016

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    Astrocytes are the most abundant neuron-supporting glial cells in the central nervous system. The neuroprotective role of astrocytes has been demonstrated in various neurological disorders such as amyotrophic lateral sclerosis, spinal cord injury, stroke and Parkinson's disease (PD). Astrocyte dysfunction or loss-of-astrocytes increases the susceptibility of neurons to cell death, while astrocyte transplantation in animal studies has therapeutic advantage. We reported recently that stimulation of serotonin 1A (5-HT1A) receptors on astrocytes promoted astrocyte proliferation and upregulated antioxidative molecules to act as a neuroprotectant in parkinsonian mice. PD is a progressive neurodegenerative disease with motor symptoms such as tremor, bradykinesia, rigidity and postural instability, that are based on selective loss of nigrostriatal dopaminergic neurons, and with non-motor symptoms such as orthostatic hypotension and constipation based on peripheral neurodegeneration. Although dopaminergic therapy for managing the motor disability associated with PD is being assessed at present, the main challenge remains the development of neuroprotective or disease-modifying treatments. Therefore, it is desirable to find treatments that can reduce the progression of dopaminergic cell death. In this article, we summarize first the neuroprotective properties of astrocytes targeting certain molecules related to PD. Next, we review neuroprotective effects induced by stimulation of 5-HT1A receptors on astrocytes. The review discusses new promising therapeutic strategies based on neuroprotection against oxidative stress and prevention of dopaminergic neurodegeneration.

    DOI: 10.2174/0929867323666160122115057

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  • Changes in Metallothionein Isoform Expression in the Bones of Ovariectomized Rats Reviewed

    Chiharu Sogawa, Mika Ikegame, Ikuko Miyazaki, Toshiaki Ara, Yasuhiro Imamura, Yuka Okusha, Kazumi Ohyama, Masato Asanuma, Norio Sogawa, Toshio Yamamoto, Ken-ichi Kozaki

    Journal of Hard Tissue Biology   25 ( 1 )   21 - 26   2016

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    DOI: 10.2485/jhtb.25.21

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  • Serotonin-1A agonist 8-OH-DPAT alleviates motor dysfunction and motor neuron degeneration in a model of amyotrophic lateral sclerosis. Reviewed

    Ikuko Miyazaki, Shinki Murakami, Takashi Nakano, Nao Torigoe, Ryo Kikuoka, Yoshihisa Kitamura, Toshiaki Sendo, Masato Asanuma

    Annals of Pharmacology and Pharmaceutics   1 ( 1 )   1003   2016

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  • Doxorubicin and cyclophosphamide treatment produces anxiety-like behavior and spatial cognition impairment in rats: Possible involvement of hippocampal neurogenesis via brain-derived neurotrophic factor and cyclin D1 regulation Reviewed

    Yoshihisa Kitamura, Sayo Hattori, Saori Yoneda, Saori Watanabe, Erika Kanemoto, Misaki Sugimoto, Toshiki Kawai, Ayumi Machida, Hirotaka Kanzaki, Ikuko Miyazaki, Masato Asanuma, Toshiaki Sendo

    Behavioural Brain Research   292   184 - 193   2015.10

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    DOI: 10.1016/j.bbr.2015.06.007

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  • Long-Term Systemic Exposure to Rotenone Induces Central and Peripheral Pathology of Parkinson’s Disease in Mice Reviewed

    Shinki Murakami, Ikuko Miyazaki, Ko Miyoshi, Masato Asanuma

    Neurochemical Research   40 ( 6 )   1165 - 1178   2015.6

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    DOI: 10.1007/s11064-015-1577-2

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  • Possible involvement of iron-induced oxidative insults in neurodegeneration Reviewed

    Takeshi Asano, Masato Koike, Shin-ichi Sakata, Yukiko Takeda, Tomoko Nakagawa, Taku Hatano, Satoshi Ohashi, Manabu Funayama, Kenji Yoshimi, Masato Asanuma, Shinya Toyokuni, Hideki Mochizuki, Yasuo Uchiyama, Nobutaka Hattori, Kazuhiro Iwai

    Neuroscience Letters   588   29 - 35   2015.2

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    DOI: 10.1016/j.neulet.2014.12.052

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  • ハルミンの薬物依存性ならびに細胞毒性の評価:植物由来幻覚成分の有害作用について.

    舩田正彦, 竹林美佳, 宮崎育子, 浅沼幹人, 青尾直也, 和田 清

    精神保健研究   61 ( 28 )   61 - 72   2015

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  • Visualization of Astrocytic Primary Cilia in the Mouse Brain by Immunofluorescent Analysis Using the Cilia Marker Arl13b Reviewed

    Kyosuke Kasahara, Ko Miyoshi, Shinki Murakami, Ikuko Miyazaki, Masato Asanuma

    Acta Medica Okayama   68 ( 6 )   317 - 322   2014.12

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    In vertebrates, almost all somatic cells extend a single immotile cilium, referred to as a primary cilium. Increasing evidence suggests that primary cilia serve as cellular antennae in many types of tissues by sensing chemical or mechanical stimuli in the milieu surrounding the cells. In rodents an antibody to adenylyl cyclase 3 (AC3) has been widely used to label the primary cilia of neurons in vivo by immunostaining, whereas the lack of markers for the primary cilia of astrocytes has made it difficult to observe astrocytic primary cilia in vivo. Here, we obtained a visualization of astrocytic primary cilia in the mouse brain. In the somatosensory cortex, a large portion of neurons and astrocytes at postnatal day 10 (P10), and of neurons at P56 had AC3-positive primary cilia, whereas only approx. one-half of the astrocytes in the P56 mice carried primary cilia weakly positive for AC3. In contrast, the majority of astrocytes had ADP-ribosylation factor-like protein 13B (Arl13b)-positive primary cilia in the somatosensory cortex and other brain regions of P56 mice. The lengths of astrocytic primary cilia positive for Arl13b varied among the brain regions. Our data indicate that Arl13b is a noteworthy marker of astrocytic primary cilia in the brain.

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  • Methylphenidate improves learning impairments and hyperthermia‐induced seizures caused by an S cn1a mutation Reviewed

    Iori Ohmori, Nozomi Kawakami, Sumei Liu, Haijiao Wang, Ikuko Miyazaki, Masato Asanuma, Hiroyuki Michiue, Hideki Matsui, Tomoji Mashimo, Mamoru Ouchida

    Epilepsia   55 ( 10 )   1558 - 1567   2014.10

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    DOI: 10.1111/epi.12750

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  • Neuroprotective Effects of Metallothionein Against Rotenone-Induced Myenteric Neurodegeneration in Parkinsonian Mice Reviewed

    Shinki Murakami, Ikuko Miyazaki, Norio Sogawa, Ko Miyoshi, Masato Asanuma

    Neurotoxicity Research   26 ( 3 )   285 - 298   2014.10

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    DOI: 10.1007/s12640-014-9480-1

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  • Striatal Astrocytes Act as a Reservoir for L-DOPA Reviewed

    Masato Asanuma, Ikuko Miyazaki, Shinki Murakami, Francisco J. Diaz-Corrales, Norio Ogawa

    PLoS ONE   9 ( 9 )   e106362   2014.9

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    DOI: 10.1371/journal.pone.0106362

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  • Effects of (+)-8-OH-DPAT on the duration of immobility during the forced swim test and hippocampal cell proliferation in ACTH-treated rats Reviewed

    Ayaka Miyake, Yoshihisa Kitamura, Ikuko Miyazaki, Masato Asanuma, Toshiaki Sendo

    Pharmacology Biochemistry and Behavior   122   240 - 245   2014.7

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    In the present study, we examined the effect of ACTH on the immobilization of rats in the forced swim test and hippocampal cell proliferation after administration of the 5-HT1A receptor agonist, R-(+)-8-hydroxy-2-di-n-propylamino tetralin ((+)-8-OH-DPAT). Chronic treatment with (+)-8-OH-DPAT (0.01-0.1 mg/kg, s.c.) significantly decreased the duration of immobility in saline- and ACTH-treated rats. Chronic administration of ACTH caused a significant decrease in hippocampal cell proliferation. However, (+)-8-OH-DPAT significantly normalized cell proliferation in ACTH-treated rats. We then investigated the effects of (+)-8-OH-DPAT on the expression of brain-derived neurotrophic factor (BDNF) and cyclin D1 (elements of cyclic adenosine monophosphate response element-binding protein (CREB)-BDNF and Wnt signaling pathways, respectively) in the hippocampus of saline- and ACTH-treated rats. ACTH treatment significantly decreased the expression of cyclin D1, while treatment with (+)-8-OH-DPAT normalized the expression of cyclin D1 in ACTH-treated rats. However, the expression of BDNF did not change in either saline- or ACTH-treated rats. These findings suggest that the antidepressant effects of (+)-8-OH-DPAT in treatment-resistant animals may be attributed to an enhancement of hippocampal cell proliferation, at least in part due to an enhancement of cyclin D1 expression. (C) 2014 Elsevier Inc All rights reserved.

    DOI: 10.1016/j.pbb.2014.04.003

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  • Lack of Dopaminergic Inputs Elongates the Primary Cilia of Striatal Neurons Reviewed

    Ko Miyoshi, Kyosuke Kasahara, Shinki Murakami, Mika Takeshima, Natsuko Kumamoto, Asako Sato, Ikuko Miyazaki, Shinsuke Matsuzaki, Toshikuni Sasaoka, Taiichi Katayama, Masato Asanuma

    PLoS ONE   9 ( 5 )   e97918 - e97918   2014.5

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    DOI: 10.1371/journal.pone.0097918

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  • Protective Effects of Phytochemical Antioxidants Against Neurotoxin-Induced Degeneration of Dopaminergic Neurons Reviewed

    Taizo Kita, Masato Asanuma, Ikuko Miyazaki, Mika Takeshima

    Journal of Pharmacological Sciences   124 ( 3 )   313 - 319   2014.3

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    The specific toxicity to dopaminergic neurons of psychostimulants and neurotoxins has been extensively studied in vivo and in vitro, and findings have been used to establish animal models of amphetamine psychosis or Parkinson's disease. The multiple mechanisms of neurotoxicity operating in these disorders are known to involve oxidative stress or neuroinflammation, producing the characteristic behavioral and neuropathlogical changes arising from injured dopaminergic neurons and glial cells. A number of studies have shown that glia-targeting antioxidants play important roles in protecting against the neurotoxicity caused by psychostimulants or neurotoxins. Phytochemicals, which are non-nutritive plant chemicals, protect dopaminergic neurons and glial cells from damage caused by psychostimulants or neurotoxins. The objective of this review was to evaluate the involvement of glial cells in dopaminergic neuron specific toxicity and to explore the neuroprotective activity of phytochemicals in terms of anti-inflammatory and antioxidant action.

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  • Effects of Bupropion and Pramipexole on Cell Proliferation in the Hippocampus of Adrenocorticotropic Hormone-Treated Rats Reviewed

    Yuka Onoue, Keiko Kuwatsuka, Ikuko Miyazaki, Masato Asanuma, Yoshihisa Kitamura, Toshiaki Sendo

    Biological & Pharmaceutical Bulletin   37 ( 2 )   327 - 330   2014.2

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    The dopamine reuptake inhibitor bupropion and dopamine D2/3 receptor agonist pramipexole have been clinically proven to improve both depression and treatment-resistant depression. We examined its influence on the duration of immobility during the forced swim test in adrenocorticotropic hormone (ACTH)-treated rats and further analyzed the possible role of the dopamine nerve system in this effect. Bupropion and pramipexole significantly decreased the duration of immobility in normal and ACTH-treated rats. We previously demonstrated that the chronic administration of ACTH caused a significant decrease in hippocampal cell proliferation and neurogenesis. In this study, we used the mitotic marker 5-bromo-2'-deoxyridine to investigate the effects of bupropion and pramipexole on cell proliferation in the subgranular zone of the hippocampal dentate gyms following chronic treatment with ACTH. The ACTH treatment for 14 d decreased adult hippocampal cell proliferation. The chronic administration of bupropion for 14 d blocked the loss of cell proliferation resulting from the chronic treatment with ACTH, whereas pramipexole did not. The administration of bupropion may have treatment-resistant antidepressive properties, which may be partly attributed to the normalization of hippocampal cell proliferation.

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  • Metallothionein deficiency exacerbates diabetic nephropathy in streptozotocin-induced diabetic mice Reviewed

    Hiromi Tachibana, Daisuke Ogawa, Norio Sogawa, Masato Asanuma, Ikuko Miyazaki, Naoto Terami, Takashi Hatanaka, Chikage Sato Horiguchi, Atsuko Nakatsuka, Jun Eguchi, Jun Wada, Hiroshi Yamada, Kohji Takei, Hirofumi Makino

    American Journal of Physiology-Renal Physiology   306 ( 1 )   F105 - F115   2014.1

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    Oxidative stress and inflammation play important roles in diabetic complications, including diabetic nephropathy. Metallothionein (MT) is induced in proximal tubular epithelial cells as an antioxidant in the diabetic kidney; however, the role of MT in renal function remains unclear. We therefore investigated whether MT deficiency accelerates diabetic nephropathy through oxidative stress and inflammation. Diabetes was induced by streptozotocin injection in MT-deficient (MT−/−) and MT+/+ mice. Urinary albumin excretion, histological changes, markers for reactive oxygen species (ROS), and kidney inflammation were measured. Murine proximal tubular epithelial (mProx24) cells were used to further elucidate the role of MT under high-glucose conditions. Parameters of diabetic nephropathy and markers of ROS and inflammation were accelerated in diabetic MT−/− mice compared with diabetic MT+/+ mice, despite equivalent levels of hyperglycemia. MT deficiency accelerated interstitial fibrosis and macrophage infiltration into the interstitium in the diabetic kidney. Electron microscopy revealed abnormal mitochondrial morphology in proximal tubular epithelial cells in diabetic MT−/− mice. In vitro studies demonstrated that knockdown of MT by small interfering RNA enhanced mitochondrial ROS generation and inflammation-related gene expression in mProx24 cells cultured under high-glucose conditions. The results of this study suggest that MT may play a key role in protecting the kidney against high glucose-induced ROS and subsequent inflammation in diabetic nephropathy.

    DOI: 10.1152/ajprenal.00034.2013

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  • アストロサイトによる神経機能修飾とパーキンソン病での神経保護 Invited

    浅沼幹人

    岡山医学会雑誌   126 ( 3 )   203 - 208   2014

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    DOI: 10.4044/joma.126.203

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  • お茶の旨味成分テアニンのアストログリア細胞における細胞保護効果

    喜多大三, 浅沼幹人, 宮崎育子, 竹島美香

    九州栄養福祉大学研究紀要   10   179 - 191   2013.12

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  • Targeting 5-HT1A receptors in astrocytes to protect dopaminergic neurons in parkinsonian models Reviewed

    Ikuko Miyazaki, Masato Asanuma, Shinki Murakami, Mika Takeshima, Nao Torigoe, Yoshihisa Kitamura, Ko Miyoshi

    Neurobiology of Disease   59   244 - 256   2013.11

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    Astrocytes are abundant neuron-supporting glial cells that harbor a powerful arsenal of neuroprotective antioxidative molecules and neurotrophic factors. Here we examined whether enrichment with healthy striatal astrocytes can provide neuroprotection against progressive dopaminergic neurodegeneration. Serotonin 1A (5-HT1A) agonist 8-OH-DPAT induced astrocyte proliferation and increased metallothionein-1/-2 (MT-1/-2), antioxidative molecules, in cultured astrocytes and the striatum of mice. Primary cultured mesencephalic dopamine neurons were protected against oxidative stress by preincubation with conditioned media from 8-OH-DPAT-treated astrocytes. These protective effects were canceled by 5-HT1A antagonist or MT-1/-2-specific antibody. Furthermore, reduction of nigrostriatal dopaminergic neurons in 6-hydroxydopamine-lesioned parkinsonian model mice was significantly abrogated by repeated injections of 8-OH-DPAT. Treatment with 8-OH-DPAT markedly increased the expression of MT in striatal astrocytes in the hemi-parkinsonian mice. Our study provides a promising therapeutic strategy of neuroprotection against oxidative stress and progressive dopaminergic neurodegeneration by demonstrating the efficacy of targeting 5-HT1A receptors in astrocytes. © 2013 Elsevier Inc.

    DOI: 10.1016/j.nbd.2013.08.003

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  • Transplantation of Melanocytes Obtained from the Skin Ameliorates Apomorphine-Induced Abnormal Behavior in Rodent Hemi-Parkinsonian Models Reviewed

    Masato Asanuma, Ikuko Miyazaki, Francisco J. Diaz-Corrales, Youichirou Higashi, Masayoshi Namba, Norio Ogawa

    PLoS ONE   8 ( 6 )   e65983 - e65983   2013.6

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    DOI: 10.1371/journal.pone.0065983

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  • Protective effect of cepharanthin on cisplatin-induced renal toxicity through metallothionein expression Reviewed

    Norio Sogawa, Kanji Hirai, Chiharu Sogawa, Kazumi Ohyama, Ikuko Miyazaki, Goichi Tsukamoto, Masato Asanuma, Akira Sasaki, Shigeo Kitayama

    Life Sciences   92 ( 12 )   727 - 732   2013.4

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    Aims Cisplatin (CDDP) is a potent anticancer agent, but severe renal toxicity can limit its use. We investigated the protective effect of cepharanthin (CE), a biscoclaurin alkaloid, on the renal toxicity of CDDP. Main methods Mice were given CDDP along with CE. Effects of CE on CDDP toxicity were investigated by assaying markers of renal toxicity together with MT expression, and by histopathological examination of the kidney. MT-null mice were also examined. Key findings CE induced expression of metallothionein (MT). Pre-administration of CE attenuated an increase in blood urea nitrogen (BUN) concentrations after the CDDP injection. A histochemical analysis demonstrated protection against CDDP-induced necrocytosis of kidney tissues by CE. The protective effect of CE did not occur in the MT-null mice. Significance Pretreatment with CE may reduce the renal toxicity of CDDP through expression of MT. © 2013 Elsevier Inc.

    DOI: 10.1016/j.lfs.2013.01.031

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  • アストロサイトとParkinson病治療 Invited

    浅沼幹人, 宮崎育子

    神経内科   79 ( 2 )   257 - 261   2013

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  • The mechanisms of electroconvulsive stimuli in BrdU-positive cells of the dentate gyrus in ACTH-treated rats Reviewed

    Keiko Kuwatsuka, Hiromi Hayashi, Yuka Onoue, Ikuko Miyazaki, Toshihiro Koyama, Masato Asanuma, Yoshihisa Kitamura, Toshiaki Sendo

    Journal of Pharmacological Sciences   122 ( 1 )   34 - 41   2013

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    In clinical studies, electroconvulsive stimuli have been associated with improvements in both depression and treatment-resistant depression. In a previous study, treatment with adrenocorticotropic hormone (ACTH) for 14 days decreased adult hippocampal cell proliferation. Furthermore, electroconvulsive stimuli significantly decreased the duration of immobility following repeated administration of ACTH for 14 days in rats. The present study was undertaken to further characterize the mechanism of treatment-resistant antidepressant effects of electroconvulsive stimuli by measuring cell proliferation, brain-derived neurotrophic factor (BDNF) levels, and phosphorylated and total cyclic adenosine monophosphate (cAMP) response element-binding protein (pCREB/CREB) levels in the hippocampus of ACTH-treated rats. Electroconvulsive stimuli increased cell proliferation in both saline-treated and ACTH-treated rats. Mature-BDNF protein levels showed a tendency to decrease in ACTH-treated rats. Electroconvulsive stimuli treatment increased mature-BDNF protein levels in the hippocampus of both saline-treated and ACTH-treated rats. Furthermore, electroconvulsive stimuli increased phospho-Ser133-CREB (pCREB) levels and the ratio of pCREB/CREB in both saline-treated and ACTH-treated rats. These findings suggest that the treatment-resistant antidepressant effects of electroconvulsive stimuli may be attributed, at least in part, to an enhancement of hippocampal cell proliferation. © The Japanese Pharmacological Society.

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  • テアニンの中枢作用に関する文献的考察.

    喜多大三, 浅沼幹人, 宮崎育子, 竹島美香

    九州栄養福祉大学研究紀要   9   45 - 58   2012.12

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  • Centrosomal aggregates and Golgi fragmentation disrupt vesicular trafficking of DAT Reviewed

    Francisco J. Diaz-Corrales, Ikuko Miyazaki, Masato Asanuma, Diego Ruano, Rosa M. Rios

    Neurobiology og Aging   33 ( 10 )   2462 - 2477   2012.10

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    Lewy bodies containing the centrosomal protein gamma-tubulin and fragmentation of Golgi apparatus (GA) have been described in nigral neurons of Parkinson's disease (PD) patients. However, the relevance of these features in PD pathophysiology remains unknown. We analyzed the impact of proteasome inhibition in the formation of gamma-tubulin-containing aggregates as well as on GA structure. SH-SY5Y cells were treated with the proteasome inhibitor Z-Leu-Leu-Leu-al (MG132) to induce centrosomal-protein aggregates. Then, microtubules (MTs) and Golgi dynamics, as well as the vesicular transport of dopamine transporter (DAT) were evaluated both in vitro and in living cells. MG132 treatment induced gamma-tubulin aggregates which altered microtubule nucleation. MG132-treated cells containing gamma-tubulin aggregates showed fragmentation of GA and perturbation of the trans-Golgi network. Under these conditions, the DAT accumulated at the centrosomal-Golgi region indicating that the vesicular transport of DAT was disrupted. Thus, centrosomal aggregates and fragmentation of GA are 2 closely related processes that could result in the disruption of the vesicular transport of DAT toward the plasma membrane in a model of dopaminergic neuronal degeneration. (C) 2012 Elsevier Inc. All rights reserved.

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  • Cyclooxygenase-Independent Neuroprotective Effects of Aspirin Against Dopamine Quinone-Induced Neurotoxicity Reviewed

    Masato Asanuma, Ikuko Miyazaki, Yuri Kikkawa, Naotaka Kimoto, Mika Takeshima, Shinki Murakami, Ko Miyoshi

    Neurochemical Research   37 ( 9 )   1944 - 1951   2012.9

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    Prostaglandin H synthase exerts not only cyclooxygenase activity but also peroxidase activity. The latter activity of the enzyme is thought to couple with oxidation of dopamine to dopamine quinone. Therefore, it has been proposed that cyclooxygenase inhibitors could suppress dopamine quinone formation. In the present study, we examined effects of various cyclooxygenase inhibitors against excess methyl L-3,4-dihydroxyphenylalanine (L-DOPA)-induced quinoprotein (protein-bound quinone) formation and neurotoxicity using dopaminergic CATH.a cells. The treatment with aspirin inhibited excess methyl L-DOPA-induced quinoprotein formation and cell death. However, acetaminophen did not show protective effects, and indomethacin and meloxicam rather aggravated these methyl L-DOPA-induced changes. Aspirin and indomethacin did not affect the level of glutathione that exerts quenching dopamine quinone in dopaminergic cells. In contrast with inhibiting effects of higher dose in the previous reports, relatively lower dose of aspirin that affected methyl L-DOPA-induced quinoprotein formation and cell death failed to prevent cyclooxygenase-induced dopamine chrome generation in cell-free system. Furthermore, aspirin but not acetaminophen or meloxicam showed direct dopamine quinone-scavenging effects in dopamine-semiquinone generating systems. The present results suggest that cyclooxygenase shows little contribution to dopamine oxidation in dopaminergic cells and that protective effects of aspirin against methyl L-DOPA-induced dopamine quinone neurotoxicity are based on its cyclooxygenase-independent property.

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  • Effluent free radicals are associated with residual renal function and predict technique failure in peritoneal dialysis patients. Reviewed

    Hiroshi Morinaga, Hitoshi Sugiyama, Tatsuyuki Inoue, Keiichi Takiue, Yoko Kikumoto, Masashi Kitagawa, Shigeru Akagi, Kazushi Nakao, Yohei Maeshima, Ikuko Miyazaki, Masato Asanuma, Makoto Hiramatsu, Hirofumi Makino

    Peritoneal Dialysis International   32 ( 4 )   453 - 461   2012.7

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    Objective: Residual renal function (RRF) is associated with low oxidative stress in peritoneal dialysis (PD). In the present study, we investigated the relationship between the impact of oxidative stress on RRF and patient outcomes during PD.
    Methods: Levels of free radicals (FRs) in effluent from the overnight dwell in 45 outpatients were determined by electron spin resonance spectrometry. The FR levels, clinical parameters, and the level of 8-hydroxy-2'-deoxyguanosine were evaluated at study start. The effects of effluent FR level on technique and patient survival were analyzed in a prospective cohort followed for 24 months.
    Results: Levels of effluent FRs showed significant negative correlations with daily urine volume and residual renal Kt/V, and positive correlations with plasma beta(2)-microglobulin and effluent 8-hydroxy-2'-deoxyguanosine. A highly significant difference in technique survival (p &lt; 0.05), but not patient survival, was observed for patients grouped by effluent FR quartile. The effluent FR level was independently associated with technique failure after adjusting for patient age, history of cardiovascular disease, and presence of diabetes mellitus (p &lt; 0.001). The level of effluent FRs was associated with death-censored technique failure in both univariate (p &lt; 0.001) and multivariate (p &lt; 0.01) hazard models. Compared with patients remaining on PD, those withdrawn from the modality had significantly higher levels of effluent FRs (p &lt; 0.005).
    Conclusions: Elevated effluent FRs are associated with RRF and technique failure in stable PD patients. These findings highlight the importance of oxidative stress as an unfavorable prognostic factor in PD and emphasize that steps should be taken to minimize oxidative stress in these patients. Perit Dial Int 2012; 32(4): 453-461

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  • Dipeptidyl compounds ameliorate the serum-deprivation-induced reduction in cell viability via the neurotrophin-activating effect in SH-SY5Y cells Reviewed

    Ken-ichi Tanaka, Hiroya Ogo, Hiroaki Kaji, Kaori Miyatake, Erika Tokudome, Kanako Sonoda, Norio Ogawa, Masato Asanuma

    Neurological Research   34 ( 6 )   619 - 622   2012.7

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    Objectives and methods: We have searched for low-molecular-weight compounds as potent new non-immunosuppressive immunophilin ligands (NI-IPLs) that are stronger than existent NI-IPLs such as GPI1046 and/or V10367 from the perspective of neuroprotective efficacy. We selected six dipeptidyl compounds as new NI-IPL candidates, and first examined the effects of each of these compounds on the serum-deprivation-induced reduction in the viability of SH-SY5Y cells. In addition, we clarified the effects of these compounds on neurotrophin release into medium in SH-SY5Y cells.
    Results: Pre-treatment with Leu-Ile and Ile-Ile prevented the serum deprivation-induced reduction in cell viability in SH-SY5Y cells. In naive SH-SY5Y cells, treatment with Leu-Ile and Ile-Ile for 24 hours significantly increased both brain-derived neurotrophic factor and glial cell-line-derived neurotrophic factor releases in comparison with relative vehicle treatments. Moreover, none of the dipeptidyl compounds could prevent the concanavalin A-induced enhancement in interleukin-2 and interleukin-4 release in mouse spleen cells.
    Discussion: The immunosuppressive effect is not essential to the neuroprotective properties of dipeptidyl compounds, and Leu-Ile and Ile-Ile have neurotrophin-activating effects, like FK506 and its existing non-immunosuppressive derivatives.

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  • ACTH反復投与ラットにおける海馬細胞新生の減少及びそのメカニズムに関する検討.

    林 宏美, 土居真穂, 尾上由華, 鍬塚圭子, 三宅彩香, 小山敏広, 四宮一昭, 宮崎育子, 浅沼幹人, 北村佳久

    薬学雑誌   132 ( 2 )   173 - 178   2012

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  • L-テアニンのグリア細胞に対する保護作用に関する研究─アストロサイトにおけるL-テアニンによる抗酸化保護作用の賦活─.

    喜多大三, 浅沼幹人, 宮崎育子, 竹島美香

    九州栄養福祉大学研究紀要   8   43 - 53   2011.12

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  • Protective effects of baicalein against excess L-DOPA-induced dopamine quinone neurotoxicity Reviewed

    Mika Takeshima, Maiko Murata, Natsuho Urasoe, Shinki Murakami, Ikuko Miyazaki, Masato Asanuma, Taizo Kita

    Neurological Research   33 ( 10 )   1050 - 1056   2011.12

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    Objectives: Baicalein, a flavonoid derived from the root of Scutelaria baicalensis Georgi, possesses antioxidative properties including reactive oxygen species scavenging and lipid peroxidation inhibiting activities. The present study was undertaken to investigate the neuroprotective effect of baicalein against dopamine (DA) neurotoxicity induced by exposure to a synthetic DA precursor, L-3,4-dihydroxyphenylalanine (L-DOPA), in cultured dopaminergic CATH. a cells.
    Methods and results: Exposure to L-DOPA for 24 hours reduced the number of viable cells and enhanced protein-bound quinone (quinoprotein) formation in the cell. Both effects were prevented by simultaneous treatment with baicalein. In addition, baicalein prevented the formation of DA semiquinone radicals from DA in an in vitro cell-free system. Long-term baicalein treatment for 96 hours also protected against excess L-DOPA-induced cell death, and also increased glutathione (GSH) levels in CATH. a cells.
    Discussion: Our results indicate that baicalein has neuroprotective properties against excess L-DOPA-induced DA neurotoxicity through the suppression of DA quinone formation. Furthermore, the long-term treatment of baicalein upregulates intracellular GSH contents, which may also exert neuroprotective effects against oxidative stress-induced neuronal damage.

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  • Factors That Influence Primary Cilium Length Reviewed

    Ko Miyoshi, Kyosuke Kasahara, Ikuko Miyazaki, Masato Asanuma

    Acta Medica Okayama   65 ( 5 )   279 - 285   2011.10

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    Almost all mammalian cells carry one primary cilium that functions as a biosensor for chemical and mechanical stimuli. Genetic damages that compromise cilia formation or function cause a spectrum of disorders referred to as ciliapathies. Recent studies have demonstrated that some pharmacological agents and extracellular environmental changes can alter primary cilium length. Renal injury is a well-known example of an environmental insult that triggers cilia length modification. Lithium treatment causes primary cilia to extend in several cell types including neuronal cells; this phenomenon is likely independent of glycogen synthase kinase-3 beta inhibition. In renal epithelial cell lines, deflection of the primary cilia by fluid shear shortens them by reducing the intracellular cyclic AMP level, leading to a subsequent decrease in mechanosensitivity to fluid shear. Primary cilium length is also influenced by the dynamics of actin filaments and microtubules through the levels of soluble tubulin in the cytosol available for primary cilia extension. Thus, mammalian cells can adapt to the extracellular environment by modulating the primary cilium length, and this feedback system utilizing primary cilia might exist throughout the mammalian body. Further investigation is required concerning the precise molecular mechanisms underlying the control of primary cilium length in response to environmental factors.

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  • alpha 7 Nicotinic acetylcholine receptors in the central amygdaloid nucleus alter naloxone-induced withdrawal following a single exposure to morphine Reviewed

    Shigeru Ishida, Yoichi Kawasaki, Hiroaki Araki, Masato Asanuma, Hisashi Matsunaga, Toshiaki Sendo, Hiromu Kawasaki, Yutaka Gomita, Yoshihisa Kitamura

    Psychopharmacology   214 ( 4 )   923 - 931   2011.4

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    Negative motivational withdrawal from acute opiate dependence was induced by an opioid antagonist, and the withdrawal signs prevented by pretreatment with nicotine.
    The present study was undertaken to examine the mechanism of nicotine-induced attenuation of withdrawal precipitated by naloxone in rats administered a single dose of morphine.
    Conditioned place aversion (CPA) was precipitated by naloxone in rats exposed once to morphine. Nicotinic acetylcholine receptor (nAChR) agonists were microinjected into the central amygdaloid nucleus (CeA) before naloxone was administered. Additionally, c-Fos expression in the amygdala was measured in rats exposed to alpha 7 nAChR ligands.
    The microinjection of nicotine (0.3 and 1.0 mu g/mu l) into the CeA dose-dependently inhibited naloxone-induced CPA. This inhibition of CPA was reversed by methyllycaconitine (MLA), an alpha 7 nAChR antagonist. CPA was also significantly attenuated by the microinjection of tropisetron (3.0 mu g/mu l), an alpha 7 nAChR agonist and 5-hydroxytriptamine 3 (5-HT3) receptor antagonist, but not by ondansetron (1.0 and 3.0 mu g/mu l), a 5-HT3 receptor antagonist. The microinjection of PNU-282987 (3.0 mu g/mu l), a selective alpha 7 nAChR agonist, into the CeA also inhibited CPA. Furthermore, nicotine increased c-Fos expression in the CeA, but not the medial or basolateral amygdaloid nucleus. The increase of c-Fos in the CeA was significantly inhibited by MLA.
    Nicotine-induced attenuation of CPA precipitated by naloxone is mediated by the alpha 7 nAChR subtype, and the CeA is one of the regions of the brain involved in the effect of nicotine on acutely opiate-dependent subjects.

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  • Astrocyte-Derived Metallothionein Protects Dopaminergic Neurons from Dopamine Quinone Toxicity Reviewed

    Ikuko Miyazaki, Masato Asanuma, Yuri Kikkawa, Mika Takeshima, Shinki Murakami, Ko Miyoshi, Norio Sogawa, Taizo Kita

    Glia   59 ( 3 )   435 - 451   2011.3

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    Our previous studies demonstrated the involvement of quinone formation in dopaminergic neuron dysfunction in the L-DOPA-treated parkinsonian model and in methamphetamine (METH) neurotoxicity. We further reported that the cysteine-rich metal-binding metallothionein (MT) family of proteins protects dopaminergic neurons against dopamine (DA) quinone neurotoxicity by its quinone-quenching property. The aim of this study was to examine MT induction in astrocytes in response to excess DA and the potential neuroprotective effects of astrocyte-derived MTs against DA quinone toxicity. DA exposure significantly upregulated MT-1/-2 in cultured striatal astrocytes, but not in mesencephalic neurons. This DA-induced MT upregulation in astrocytes was blocked by treatment with a DA-transporter (DAT) inhibitor, but not by DA-receptor antagonists. Expression of nuclear factor erythroid 2-related factor (Nrf2) and its binding activity to antioxidant response element of MT-1 gene were significantly increased in the astrocytes after DA exposure. Nuclear translocation of Nrf2 was suppressed by the DAT inhibitor. Quinone formation and reduction of mesencephalic DA neurons after DA exposure were ameliorated by preincubation with conditioned media from DA-treated astrocytes. These protective effects were abrogated by MT-1/-2-specific antibody. Adding exogenous MT-1 to glial conditioned media also showed similar neuroprotective effects. Furthermore, MT-1/-2 expression was markedly elevated specifically in reactive astrocytes in the striatum of L-DOPA-treated hemi-parkinsonian mice or METH-injected mice. These results suggested that excess DA taken up by astrocytes via DAT upregulates MT-1/-2 expression specifically in astrocytes, and that MTs or related molecules secreted specifically by astrocytes protect dopaminergic neurons from damage through quinone quenching and/or scavenging of free radicals. (C)2010 Wiley-Liss, Inc.

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  • Chronic Treatment with Imipramine and Lithium Increases Cell Proliferation in the Hippocampus in Adrenocorticotropic Hormone-Treated Rats Reviewed

    Yoshihisa Kitamura, Maho Doi, Keiko Kuwatsuka, Yuka Onoue, Ikuko Miyazaki, Kazuaki Shinomiya, Toshihiro Koyama, Toshiaki Sendo, Hiromu Kawasaki, Masato Asanuma, Yutaka Gomita

    Biological & Pharmaceutical Bulletin   34 ( 1 )   77 - 81   2011.1

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    Adult hippocampal neurogenesis is reported to change in animal models of depression and antidepressants. We have used the mitotic marker 5-bromo-2'-deoxyyridine to address the effects of imipramine and lithium on cell proliferation and survival following chronic treatment with adrenocorticotropic hormone (ACTH) in the subgranular zone of the hippocampal dentate gyrus. ACTH treatment for 14d decreased adult hippocampal cell proliferation and survival. Coadministration of imipramine and lithium for 14d blocked the loss of cell proliferation but not cell survival resulting from the chronic treatment with ACTH. The coadministration of imipramine and lithium may have treatment-resistant antidepressive properties, which may be attributed, in part, to a normalization of hippocampal cell proliferation.

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  • パーキンソン病とアストロサイト─新たな神経保護療法の標的. Invited

    浅沼幹人, 宮崎育子

    Clinical Neuroscience   29 ( 11 )   1295 - 1297   2011

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  • High glucose increases metallothionein expression in renal proximal tubular epithelial cells. Reviewed

    Daisuke Ogawa, Masato Asanuma, Ikuko Miyazaki, Hiromi Tachibana, Jun Wada, Norio Sogawa, Takeshi Sugaya, Shinji Kitamura, Yohei Maeshima, Kenichi Shikata, Hirofumi Makino

    Experimental Diabetes Research   2011   534872 - 534872   2011

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    Metallothionein(MT) is an intracellular metal-binding, cysteine-rich protein, and is a potent antioxidant that protects cells and tissues from oxidative stress. Although the major isoforms MT-1 and -2 (MT-1/-2) are highly inducible in many tissues, the distribution and role of MT-1/-2 in diabetic nephropathy are poorly understood. In this study, diabetes was induced in adult male rats by streptozotocin, and renal tissues were stained with antibodies for MT-1/-2. MT-1/-2 expression was also evaluated in mProx24 cells, a mouse renal proximal tubular epithelial cell line, stimulated with high glucose medium and pretreated with the antioxidant vitamin E. MT-1/-2 expression was gradually and dramatically increased, mainly in the proximal tubular epithelial cells and to a lesser extent in the podocytes in diabetic rats, but was hardly observed in control rats. MT-1/-2 expression was also increased by high glucose stimulation in mProx24 cells. Because the induction of MT was suppressed by pretreatment with vitamin E, the expression of MT-1/-2 is induced, at least in part, by high glucose-induced oxidative stress. These observations suggest that MT-1/-2 is induced in renal proximal tubular epithelial cells as an antioxidant to protect the kidney from oxidative stress, and may offer a novel therapeutic target against diabetic nephropathy.

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  • Effects of Imipramine and Lithium on the Suppression of Cell Proliferation in the Dentate Gyrus of the Hippocampus in Adrenocorticotropic Hormone-treated Rats Reviewed

    Maho Doi, Ikuko Miyazaki, Tomoko Nagamachi, Kazuaki Shinomiya, Hisashi Matsunaga, Toshiaki Sendo, Hiromu Kawasaki, Masato Asanuma, Yutaka Gomita, Yoshihisa Kitamura

    Acta Medica Okayama   64 ( 4 )   219 - 223   2010.8

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    We examined the influence of chronic adrenocorticotropic hormone (ACTH) treatment on the number of Ki-67-positive cells in the dentate gyrus of the hippocampus in rats. ACTH treatment for 14 days decreased the number of such cells. The administration of imipramine or lithium alone for 14 days had no effect in saline-treated rats. The effect of ACTH was blocked by the administration of imipramine. Furthermore, the coadministration of imipramine and lithium for 14 days significantly increased the number of Ki-67-positive cells in both the saline and ACTH-treated rats. The coadministration of imipramine and lithium normalized the cell proliferation in the dentate gyrus of the hippocampus in rats treated with ACTH.

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  • Effects of bupropion on the forced swim test and release of dopamine in the nucleus accumbens in ACTH-treated rats Reviewed

    Yoshihisa Kitamura, Takahiko Yagi, Kouhei Kitagawa, Kazuaki Shinomiya, Hiromu Kawasaki, Masato Asanuma, Yutaka Gomita

    Naunyn-Schmiedebergs Archives of Pharmacology   382 ( 2 )   151 - 158   2010.8

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    The dopamine reuptake inhibitor bupropion has clinically been proven to improve depression and treatment-resistant depression. We examined its influence on the duration of immobility during the forced swim test in adrenocorticotropic hormone (ACTH)-treated rats and further analyzed the possible role of dopamine receptors in this effect. Additionally, the mechanism by which bupropion acts in this model was explored specifically in relation to the site of action through the use of microinjections into the medial prefrontal cortex and nucleus accumbens. Bupropion significantly decreased the duration of immobility in normal and ACTH-treated rats. This effect was blocked by D2 and D3 receptor antagonists in normal rats. Furthermore, infusions of bupropion into the nucleus accumbens, but not medial prefrontal cortex, decreased the immobility of normal and ACTH-treated rats during the forced swim test. Bupropion treatment plus repeated ACTH treatment significantly increased the extracellular dopamine concentration. These findings suggest the antidepressant-like effect of bupropion to be related to levels of dopamine in the rat nucleus accumbens.

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  • Induction of Parkinsonism-Related Proteins in the Spinal Motor Neurons of Transgenic Mouse Carrying a Mutant SOD1 Gene Reviewed

    Nobutoshi Morimoto, Makiko Nagai, Kazunori Miyazaki, Yasuyuki Ohta, Tomoko Kurata, Yasushi Takehisa, Yoshio Ikeda, Tohru Matsuura, Masato Asanuma, Koji Abe

    Journal of Neuroscience Research   88 ( 8 )   1804 - 1811   2010.6

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    Amyotrophic lateral sclerosis is a progressive and fatal disease caused by selective death of motor neurons, and a number of these patients carry mutations in the superoxide dismutase 1 (SOD1) gene involved in ameliorating oxidative stress. Recent studies indicate that oxidative stress and disruption of mitochondrial homeostasis is a common mechanism for motor neuron degeneration in amyotrophic lateral sclerosis and the loss of midbrain dopamine neurons in Parkinson&apos;s disease. Therefore, the present study investigated the presence and alterations of familial Parkinson&apos;s disease-related proteins, PINK1 and DJ-1, in spinal motor neurons of G93ASOD1 transgenic mouse model of amyotrophic lateral sclerosis. Following onset of disease, PINK1 and DJ-1 protein expression increased in the spinal motor neurons. The activated form of p53 also increased and translocated to the nuclei of spinal motor neurons, followed by increased expression of p53-activated gene 608 (PAG608). This is the first report demonstrating that increased expression of PAG608 correlates with activation of phosphorylated p53 in spinal motor neurons of an amyotrophic lateral sclerosis model. These results provide further evidence of the profound correlations between spinal motor neurons of amyotrophic lateral sclerosis and parkinsonism-related proteins. (C) 2010 Wiley-Liss, Inc.

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  • Neuroprotective Effects of Zonisamide Target Astrocyte Reviewed

    Masato Asanuma, Ikuko Miyazaki, Francisco J. Diaz-Corrales, Naotaka Kimoto, Yuri Kikkawa, Mika Takeshima, Ko Miyoshi, Miho Murata

    Annals of Neurology   67 ( 2 )   239 - 249   2010.2

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    Objective: Recent double-blind, controlled trials in Japan showed that the antiepileptic agent zonisamide (ZNS)improves the cardinal symptoms of Parkinson&apos;s disease. Glutathione (GSH) exerts antioxidative activity through quenching reactive oxygen species and dopamine quinone. GSH depletion within dopaminergic neurons impairs mitochondrial complex I activity, followed by age-dependent nigrostriatal neurodegeneration. This study examined changes in GSH and GSH synthesis-related molecules, and the neuroprotective effects of ZNS on dopaminergic neurodegeneration using 6-hydroxydopamine-injected hemiparkinsonian mice brain and cultured neurons or astrocytes.
    Methods and Results: ZNS increased both the cell number and GSH levels in astroglial C6 cells, but not in dopaminergic neuronal CATH.a cells. Repeated injections of ZNS (30mg/kg intraperitoneally) for 14 days also significantly increased GSH levels and S100 beta-positive astrocytes in mouse basal ganglia. Repeated ZNS injections (30mg/kg) for 7 days in the hemiparkinsonian mice increased the expression of cystine/glutamate exchange transporter xCT in activated astrocytes, which supply cysteine to neurons for GSH synthesis. Treatment of these mice with ZNS also increased GSH levels and completely suppressed striatal levodopa-induced quinone formation. Reduction of nigrostriatal dopamine neurons in the lesioned side of hemiparkinsonian mice was significantly abrogated by repeated injections of ZNS with or without adjunctive levodopa starting 3 weeks after 6-hydroxydopamine lesioning.
    Interpretation: These results provide new pharmacological evidence for the effects of ZNS. ZNS markedly increased GSH levels by enhancing the astroglial cystine transport system and/or astroglial proliferation via S100 beta production or secretion. ZNS acts as a neuroprotectant against oxidative stress and progressive dopaminergic neurodegeneration. ANN NEUROL 2010;67:239-249

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  • A study on bioactivity and function of chemical compounds in food and foodstuff: Search for angiotensin I-converting enzyme inhibitory substances in some edible mushrooms using fluorescent substrate.

    Haruhiko Aoyagi, Yumiyo Tsukamoto, Chiho Furuno, Setsuko Ando, Kouki Matsubara, Taizo Kita, Masato Asanuma

    九州栄養福祉大学研究紀要   6   9 - 20   2009.12

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  • 食材及び食品に含まれる化学物質の生理活性とその機能─ドパミン神経培養系におけるフィチン酸の作用─

    浦添夏帆, 村田麻衣子, 青柳東彦, 安東勢津子, 宮崎育子, 浅沼幹人, 喜多大三

    九州栄養福祉大学研究紀要   6   75 - 86   2009.12

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  • Lithium treatment elongates primary cilia in the mouse brain and in cultured cells Reviewed

    Ko Miyoshi, Kyosuke Kasahara, Ikuko Miyazaki, Masato Asanuma

    Biochemical and Biophysical Research Communications   388 ( 4 )   757 - 762   2009.10

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    The molecular mechanisms underlying the therapeutic effects of lithium, a first-line antimanic mood stabilizer, have not yet been fully elucidated. Treatment of the algae Chlamydomonas reinhardtii with lithium has been shown to induce elongation of their flagella, which are analogous structures to vertebrate cilia. In the mouse brain, adenylyl cyclase 3 (AC3) and certain neuropeptide receptors colocalize to the primary cilium of neuronal cells, suggesting a chemosensory function for the primary cilium in the nervous system. Here we show that lithium treatment elongates primary cilia in the mouse brain and in cultured cells. Brain sections from mice chronically fed with Li(2)CO(3) were subjected to immunofluorescence study. Primary cilia carrying both AC3 and the receptor for melanin-concentrating hormone (MCH) were elongated in the dorsal striatum and nucleus accumbens of lithium-fed mice, as compared to those of control animals. Moreover, lithium-treated NIH3T3 cells and cultured striatal neurons exhibited elongation of the primary cilia. The present results provide initial evidence that a psychotropic agent can affect ciliary length in the central nervous system, and furthermore suggest that lithium exerts its therapeutic effects via the upregulation of cilia-mediated MCH sensing. These findings thus contribute novel insights into the pathophysiology of bipolar mood disorder and other psychiatric diseases. (C) 2009 Elsevier Inc. All rights reserved.

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  • Effects of galantamine on L-NAME-induced behavioral impairment in Y-maze task in mice Reviewed

    Ken-ichi Tanaka, Takao Yagi, Ryosuke Shimakoshi, Koji Azuma, Takeshi Nanba, Hiroya Ogo, Akiko Tamura, Masato Asanuma

    Neuroscience Letters   462 ( 3 )   235 - 238   2009.10

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    Nitric oxide (NO) may play a role in the established processes of learning and memory. We examined the effects of N-omega-nitro-L-arginine methylester (L-NAME), a nonselective inhibitor of NO synthase (NOS), on the performance of mice in a Y-maze task. L-NAME (100 mg/kg) markedly impaired spontaneous alternation behavior. However, galantamine (0.5 mg/kg) significantly attenuated this L-NAME-induced impairment. To clarify the molecular basis underlying galantamine's protective effects against L-NAME-induced impairment of spontaneous alternation behavior, we tested the ability of mecamylamine, an antagonist of nicotinic ACh receptor (nAChR), and scopolamine, an antagonist of muscarinic ACh receptor, to reduce galantamine's protective effects, and found that only the former had such an ability. Galantamine significantly also reduced L-NAME-induced decreases in NOx levels. However, mecamylamine cancelled galantamine's efficacy in countering the L-NAME-induced decrease in NOx levels. In the present study, we have determined that galantamine's protection against L-NAME-induced impairment of spontaneous alternation behavior in the Y-maze task might be mediated mainly by NOergic activation via the nAChR-related pathway. (c) 2009 Elsevier Ireland Ltd. All rights reserved.

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  • Pericentrin, a centrosomal protein related to microcephalic primordial dwarfism, is required for olfactory cilia assembly in mice Reviewed

    Ko Miyoshi, Kyosuke Kasahara, Ikuko Miyazaki, Shoko Shimizu, Manabu Taniguchi, Shinsuke Matsuzaki, Masaya Tohyama, Masato Asanuma

    FASEB Journal   23 ( 10 )   3289 - 3297   2009.10

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    The Drosophila pericentrin-like protein has been shown to be essential for the formation of the sensory cilia of chemosensory and mechanosensory neurons by mutant analysis in flies, while the in vivo function of pericentrin, a well-studied mammalian centrosomal protein related to microcephalic primordial dwarfism, has been unclear. To determine whether pericentrin is required for ciliogenesis in mammals, we generated and analyzed mice with a hypomorphic mutation of Pcnt encoding the mouse pericentrin. Immunofluorescence analysis demonstrated that olfactory cilia of chemosensory neurons in the nasal olfactory epithelium were malformed in the homozygous mutant mice. On the other hand, the assembly of motile and primary cilia of non-neuronal epithelial cells and the formation of sperm flagella were not affected in the Pcnt-mutant mice. The defective assembly of olfactory cilia in the mutant was apparent from birth. The mutant animals displayed reduced olfactory performance in agreement with the compromised assembly of olfactory cilia. Our findings suggest that pericentrin is essential for the assembly of chemosensory cilia of olfactory receptor neurons, but it is not globally required for cilia formation in mammals.-Miyoshi, K., Kasahara, K., Miyazaki, I., Shimizu, S., Taniguchi, M., Matsuzaki, S., Tohyama, M., Asanuma, M. Pericentrin, a centrosomal protein related to microcephalic primordial dwarfism, is required for olfactory cilia assembly in mice. FASEB J. 23, 3289-3297 ( 2009). www.fasebj.org

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  • Effects of pramipexole on the duration of immobility during the forced swim test in normal and ACTH-treated rats Reviewed

    Kouhei Kitagawa, Yoshihisa Kitamura, Toshiaki Miyazaki, Junya Miyaoka, Hiromu Kawasaki, Masato Asanuma, Toshiaki Sendo, Yutaka Gomita

    Naunyn-Schmiedebergs Archives of Pharmacology   380 ( 1 )   59 - 66   2009.7

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    The dopamine D2/D3 receptor agonist pramipexole has clinically been proven to improve depression or treatment-resistant depression. However, the involvement of the dopamine receptor system on the effect of pramipexole on depression remains unclear. We examined the influence of pramipexole on the duration of immobility during the forced swim test in normal and adrenocorticotropic hormone (ACTH)-treated rats and further analyzed the possible role of dopamine receptors in this effect. Additionally, the mechanism by which pramipexole acts in this model was explored specifically in relation to the site of action through the use of microinjections into the intramedial prefrontal cortex and nucleus accumbens. Pramipexole (0.3-1 mg/kg) significantly decreased the duration of immobility in normal and ACTH-treated rats. This effect was blocked by L-741,626, a D2 receptor antagonist, and nafadotride, a D3 receptor antagonist, in normal rats. Furthermore, infusions of pramipexole into the intranucleus accumbens, but not the medial prefrontal cortex, decreased the immobility of normal and ACTH-treated rats during the forced swim test. Taken together, the results of these experiments suggested that pramipexole, administered into the intranucleus accumbens rather than the medial prefrontal cortex, exerted an antidepressant-like effect on ACTH-treated rats via the dopaminergic system. The immobility-decreasing effect of pramipexole may be mediated by dopamine D2 and D3 receptors.

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  • Approaches to Prevent Dopamine Quinone-Induced Neurotoxicity Reviewed

    Ikuko Miyazaki, Masato Asanuma

    Neurochemical Research   34 ( 4 )   698 - 706   2009.4

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    Dopamine (DA) and its metabolites containing two hydroxyl residues exert cytotoxicity in dopaminergic neuronal cells, primarily due to the generation of highly reactive DA and DOPA quinones. Quinone formation is closely linked to other representative hypotheses such as mitochondrial dysfunction, inflammation, oxidative stress, and dysfunction of the ubiquitin-proteasome system, in the pathogenesis of neurodegenerative diseases such as Parkinson&apos;s disease and methamphetamine-induced neurotoxicity. Therefore, pathogenic effects of the DA quinone have focused on dopaminergic neuron-specific oxidative stress. Recently, various studies have demonstrated that some intrinsic molecules and several drugs exert protective effects against DA quinone-induced damage of dopaminergic neurons. In this article, we review recent studies on some neuroprotective approaches against DA quinone-induced dysfunction and/or degeneration of dopaminergic neurons.

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  • Reduction of Nuclear Peroxisome Proliferator-Activated Receptor gamma Expression in Methamphetamine-Induced Neurotoxicity and Neuroprotective Effects of Ibuprofen Reviewed

    Takeshi Tsuji, Masato Asanuma, Ikuko Miyazaki, Ko Miyoshi, Norio Ogawa

    Neurochemical Research   34 ( 4 )   764 - 774   2009.4

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    We examined changes in nuclear peroxisome proliferator-activated receptor gamma (PPAR gamma) in the striatum in methamphetamine (METH)-induced dopaminergic neurotoxicity, and also examined effects of treatment with drugs possessing PPAR gamma agonistic properties. The marked reduction of nuclear PPAR gamma-expressed cells was seen in the striatum 3 days after METH injections (4 mg/kg x 4, i.p. with 2-h interval). The reduction of dopamine transporter (DAT)-positive signals and PPAR gamma expression, and accumulation of activated microglial cells were significantly and dose-dependently attenuated by four injections of a nonsteroidal anti-inflammatory drug and a PPAR gamma ligand, ibuprofen (10 or 20 mg/kg x 4, s.c.) given 30 min prior to each METH injection, but not by either a low or high dose of aspirin. Either treatment of ibuprofen or aspirin, that showed no effects on METH-induced hyperthermia, significantly blocked the METH-induced striatal cyclooxygenase (COX) expression. Furthermore, the treatment of an intrinsic PPAR gamma ligand 15d-PG J2 also attenuated METH injections-induced reduction of striatal DAT. Therefore, the present study suggests the involvement of reduction of PPAR gamma expression in METH-induced neurotoxicity. Taken together with the previous report showing protective effects of other PPAR gamma ligand, these results imply that the protective effects of ibuprofen against METH-induced neurotoxicity may be based, in part, on its anti-inflammatory PPAR gamma agonistic properties, but not on its COX-inhibiting property or hypothermic effect.

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  • Dopamine-Induced Behavioral Changes and Oxidative Stress in Methamphetamine-Induced Neurotoxicity Reviewed

    Taizo Kita, Ikuko Miyazaki, Masato Asanuma, Mika Takeshima, George C. Wagner

    International Review of Neurobiology   88   43 - 64   2009

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    DOI: 10.1016/s0074-7742(09)88003-3

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  • テアニンの培養ドパミン神経およびグリア細胞系への作用

    染矢 恵, 竹島美香, 村田麻衣子, 宮崎育子, 浅沼幹人, 喜多大三

    九州栄養福祉大学研究紀要   5   69 - 81   2008.12

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  • Dopamine Induces Supernumerary Centrosomes and Subsequent Cell Death through Cdk2 up-Regulation in Dopaminergic Neuronal Cells Reviewed

    Francisco J. Diaz-Corrales, Masato Asanuma, Ikuko Miyazaki, Ko Miyoshi, Nobutaka Hattori, Norio Ogawa

    Neurotoxicity Research   14 ( 4 )   295 - 305   2008.12

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    Aggregation of proteins in the centrosome is implicated in the pathophysiology of Parkinson&apos;s disease. However, the relevance of the centrosome in neurodegeneration is still obscure. Centrosome duplication is initiated by the cyclin E/cyclin-dependent kinase 2 (Cdk2) complex. The present study determined changes in cyclin E or Cdk2 expression and in the centrosomal structure in dopaminergic neuronal CATH.a cells exposed to 50, 100 and 150 mu M dopamine (DA) for 24 h. DA induced significant increase in Cdk2 protein and cyclin E protein, but not cyclin a mRNA. In DA-treated cells, the intense cyclin E- and Cdk2-immunofluorescence signals were co-localized around large and supernumerary centrosomes, and these two parameters of centrosome amplification were significantly increased compared with the control. Simultaneous co-treatment with DA and a Cdk2 inhibitor blocked centrosome amplification and enhanced cell viability. Our results demonstrated that DA could lead to cyclin E accumulation and Cdk2 up-regulation triggering supernumerary centrosomes and apoptotic cell death.

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  • 食品および食材に含まれる化学物質のモノアミン神経培養系に及ぼす作用に関する研究

    村田麻衣子, 竹島美香, 染矢 恵, 宮崎育子, 浅沼幹人, 喜多大三

    九州栄養福祉大学研究紀要   5   55 - 67   2008.12

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  • Effects of HMGB1 on ischemia-reperfusion injury in the rat heart Reviewed

    Susumu Oozawa, Shuji Mori, Toru Kanke, Hideo Takahashi, Keyue Liu, Yasuko Tomono, Masato Asanuma, Ikuko Miyazaki, Masahiro Nishibori, Shunji Sano

    Circulation Journal   72 ( 7 )   1178 - 1184   2008.7

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    Background Coronary ischemia-reperfusion (I/R) injury causes cardiomyocyte necrosis in a multi-step process that includes an inflammatory reaction. A recent study has suggested that high-mobility group box 1 (HMGB 1) is a late mediator of lethal sepsis and an early mediator of inflammation and necrosis following I/R injury. In the present study a neutralizing monoclonal antibody (mAb) for HMGB1 was used to clarify the role of HMGB 1 in cardiac I/R injury.
    Methods and Results Rats underwent 30 min of left coronary artery occlusion followed by 60 min reperfusion. An intravenous injection of anti-HMGB1 mAb or control IgG was administered just before reperfusion. The infarct size was enlarged in the anti-HMGB1 mAb group in comparison with the control group (p&lt;0.05). The treatment of anti-HMGB1 mAb significantly increased the plasma troponin-T and norepinephrine (NE) content in the heart in comparison with the control (p&lt;0.05). Moreover, the production of dihydroxyphenylglycol was reduced in the anti-HMGB1-treated group (p&lt;0.05).
    Conclusion This study shows for the first time the effects of treatment with neutralizing anti-HMGB1 mAb on I/R injury in the rat heart. The findings support the novel view that I/R-induced HMGB1 may be an important factor in the modulation of interstitial NE.

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  • Dopaminergic neuron-specific oxidative stress caused by dopamine itself Reviewed

    Ikuko Miyazaki, Masato Asanuma

    Acta Medica Okayama   62 ( 3 )   141 - 150   2008.6

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    Oxidative stress, including the reactive oxygen or nitrogen species generated in the enzymatical oxidation or auto-oxidation of an excess amount of dopamine, is thought to play an important role in dopaminergic neurotoxicity. Dopamine and its metabolites containing 2 hydroxyl residues exert cytotoxicity in dopaminergic neuronal cells, primarily due to the generation of highly reactive dopamine and DOPA quinones. Dopamine and DOPA quinones may irreversibly alter protein function through the formation of 5-cysteinyl-catechols on the proteins. Furthermore, the quinone formation is closely linked to other representative hypotheses such as mitochondrial dysfunction, inflammation, oxidative stress, and dysfunction of the ubiquitin-proteasome system, in the pathogenesis of neurodegenerative diseases. Therefore, pathogenic effects of the dopamine quinone have recently focused on dopaminergic neuron-specific oxidative stress. In this article, we primarily review recent studies on the pathogenicity of quinone formation, in addition to several neuroprotective approaches against dopamine quinone-induced dysfunction of dopaminergic neurons.

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  • Nonsteroidal anti-inflammatory drugs in experimental parkinsonian models and Parkinson's disease Reviewed

    Masato Asanuma, Ikuko Miyazaki

    Current Pharmacutical Design   14 ( 14 )   1428 - 1434   2008.5

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    A number of experimental studies using parkinsonian models have revealed that nonsteroidal anti-inflammatory drugs (NSAIDs) have neuroprotective properties against dopaminergic neurotoxicity not only by their cyclooxygenase-inhibiting effect but also by other specific properties or some unknown pharmacological effects. This article reviews heterogeneous pharmacological properties of NSAIDs including inhibitory effect against nitric oxide synthesis, agonistic action for peroxisome proliferator-activated receptor or possible suppressive effects against dopamine quinone generation, and also reviews their neuroprotective effects in the experimental parkinsonian models and pathogenesis of Parkinson's disease. Several epidemiological studies recently clarified that the use of nonaspirin NSAIDs but not aspirin was associated with a lower prevalence of Parkinson's disease, in contrast with neuroprotective effects of aspirin in the experimental studies. It also discusses the discrepancy between results in the experimental parkinsonian models and epidemiological data in prevalence of Parkinson's disease on the effects of NSAIDs.

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  • Specific induction of PAG608 in cranial and spinal motor neurons of L-DOPA-treated parkinsonian rats Reviewed

    Masako Shimizu, Ikuko Miyazaki, Youichirou Higashi, Maria J. Eslava-Alva, Francisco J. Diaz-Corrales, Masato Asanuma, Norio Ogawa

    Neuroscience Research   60 ( 4 )   355 - 363   2008.4

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    We identified p53-activated gene 608 (PAG608) as a specifically induced gene in striatal tissue of L-DOPA (100 mg/kg)-injected hemi-parkinsonian rats using differential display assay. In the present study, we further examined morphological distribution of PAG608 in the central nervous system of L-DOPA-treated hemi-parkinsonian rats. PAG608 expression was markedly induced in fibers and neuronal cells of the lateral globus pallidus and reticular thalamic nucleus adjacent to internal capsule, specifically in the parkinsonian side of L-DOPA-treated models. The protein was also constitutively expressed in motor neurons specifically in either side of the pontine nucleus and motor nuclei of trigeminal and facial nerves. Furthermore, L-DOPA-induced PAG608 expression on motor neurons in the contralateral side of the ventral horn of the spinal cord and the lateral corticospinal tract without cell loss. The specific induction of PAG608 6-48 h after L-DOPA injection in the extrapyramidal tracts, pyramidal tracts and corresponding lower motor neurons of the spinal cords suggests its involvement in molecular events in stimulated motor neurons. Taken together with the constitutive expression of PAG608 in the motor nuclei of cranial nerves, PAG608 may be a useful marker of stressed or activated lower motor neurons. © 2007 Elsevier Ireland Ltd and the Japan Neuroscience Society.

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  • Increased susceptibility to oxidant-mediated tissue injury and peritoneal fibrosis in acatalasemic mice Reviewed

    Naomi Fukuoka, Hitoshi Sugiyama, Tatsuyuki Inoue, Yoko Kikumoto, Kei-ichi Takiue, Hiroshi Morinaga, Kazushi Nakao, Yohei Maeshima, Masato Asanuma, Da-Hong Wang, Keiki Ogino, Noriyoshi Masuoka, Hirofumi Makino

    American Journal of Nephrology   28 ( 4 )   661 - 668   2008.4

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    Background: Peritoneal fibrosis is a major complication leading to the loss of peritoneal function in patients undergoing peritoneal dialysis. However, the effect of catalase depletion on peritoneal fibrosis has not yet been investigated. Methods: The impact of catalase deficiency on progressive peritoneal fibrosis has been studied in homozygous acatalasemic mutant mice or control wild-type mice by intraperitoneal injection of chlorhexidine gluconate (CG) every other day for 14 days. Results: The CG injections resulted in a thicker peritoneal membrane, reflecting peritoneal fibrosis with accumulation of interstitial type I collagen, peritoneal deposition of lipid peroxidation products (4-hydroxy-2-nonenal and 4-hydroxy-2-hexenal), and an elevated level of 8-hydroxy-2&apos;-deoxyguanosine in peritoneal fluid in both mouse groups on day 14. The extent of these changes, however, was significantly higher in acatalasemic mice than in wild-type mice. The level of catalase activity remained low in the acatalasemic peritoneum without the compensatory upregulation of glutathione peroxidase, but with an insufficient upregulation of superoxide dismutase activity in CG-injected mice. Conclusions: Acatalasemia, therefore, exacerbates oxidant tissue injury and induces the peritoneum to develop irreversible fibrosis which is the most important complication of peritoneal dialysis. This study suggests that catalase plays a crucial role in the defense against oxidant-mediated peritoneal injury in a mouse peritoneal fibrosis model. Copyright (C) 2008 S. Karger AG, Basel.

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  • Protective effects of interferon-gamma against methamphetamine-induced neurotoxicity Reviewed

    Hiroaki Hozumi, Masato Asanuma, Ikuko Miyazaki, Saki Fukuoka, Yuri Kikkawa, Naotaka Kimoto, Yoshihisa Kitamura, Toshiaki Sendo, Taizo Kita, Yutaka Gomita

    Toxicology Letters   177 ( 2 )   123 - 129   2008.3

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    Repeated injections of methamphetamine (METH) cause degeneration of striatal dopaminergic nerve terminals. In the present study, we examined the effects of interferon-gamma (IFN-gamma) on METH-induced striatal neurotoxicity in mice. Intraperitoneal injection of IFN-gamma before METH injection significantly prevented METH-induced reduction of striatal dopamine transporter (DAT)-positive signals and hyperthermia. Furthermore, intracerebroventricular injection of IFN-gamma before METH treatment markedly prevented METH-induced reduction of DAT. Interestingly, central IFN-gamma injection had no effect on METH-induced hyperthermia. In addition, IFN-gamma injected centrally after METH treatment, but not systemically, 1 h after the final METH injection significantly protected against METH-induced neurotoxicity. Our results suggest that IFN-gamma injected systemically or its related molecule protects against METH-induced neurotoxicity through intracerebral molecular pathways, while it can prevent METH-induced hyperthermia through different molecular events. (C) 2008 Elsevier Ireland Ltd. All rights reserved.

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  • The roles of amino acid residues at positions 216 and 219 in the structural stability and metabolic functions of rat cytochrome P450 2D1 and 2D2 Reviewed

    Shizuo Narimatsu, Kimio Kiryu, Rei Yonemoto, Manabu Yoshino, Mitsuko Kobatake, Daichi Kazamori, Saori Hagino, Kazufumi Masuda, Takashi Katsu, Masato Asanuma, Takuya Kumamoto, Tsutomu Ishikawa, Yoshihiko Funae, Shigeru Yamano, Nobumitsu Hanioka, Shinsaku Naito

    Chemico-Biological Interactions   172 ( 1 )   11 - 21   2008.3

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    We examined the effects of the mutual substitution of amino acid residues at positions 216 and 219 between rat CYP2D1 and CYP2D2 on their microsomal contents and enzymatic functions using a yeast cell expression system and 1-metloxy-N,N- diisopropyltryptamine (5-MeO-DIPT) as a substrate. CYP2D1 has amino acid residues, leucine and valine, at positions of 216 and 219, respectively, whereas CYP2D2 has phenylalanine and aspartic acid at the same positions. In reduced carbon monoxide-difference spectroscopic analysis, the substitution of Asp-219 of CYP2D2 by valine markedly increased a peak at 450 nm and concomitantly decreased a peak at 420 nm, while the replacement of Phe-216 of CYP2D2 with leucine gave no observable change. The double substitution of Phe-216 and Asp-219 by leucine and valine, respectively, yielded a typical CYP spectrum. The substitution of Val-219 of CYP2D1 by aspartic acid decreased the CYP content to one-half, whereas the replacement of Leu-216 with phenylalanine did not have any effect. The double substitution of Leu-216 and Val-219 of CYP2D1 by phenylalanine and aspartic acid, respectively, diminished the CYP content by 90%. CYP2D1 catalyzed both 5-MeO-DIPT N-deisopropylation and O-demethylation at relatively low levels, while CYP2D2 catalyzed 5-MeO-DIPT O-demethylation efficiently. The substitution of the amino acid at position 216 substantially increased 5-MeO-DIPT oxidation activities of the two CYP2D enzymes. The replacement of the amino acid at position 219 increased the 5-MeO-DIPT O- and N-dealkylation activities of CYP2D1, whereas it decreased the 5-MeO-DIPT O-demethylation activity of CYP2D2. These results indicate that amino acid residues at positions 216 and 219 have important roles in the enzymatic functions of rat CYPD1 and CYP2D2. (C) 2007 Elsevier Ireland Ltd. All rights reserved.

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  • Oxidation of 5-methoxy-N,N-diisopropyltryptamine in rat liver microsomes and recombinant cytochrome P450 enzymes Reviewed

    Shizuo Narimatsu, Rei Yonemoto, Kazufumi Masuda, Takashi Katsu, Masato Asanuma, Tooru Kamata, Munehiro Katagi, Hitoshi Tsuchihashi, Takuya Kumamoto, Tsutomu Ishikawa, Shinsaku Naito, Shigeru Yamano, Nobumitsu Hanioka

    Biochemical Pharmacology   75 ( 3 )   752 - 760   2008.2

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    The oxidative metabolism of 5-methoxy-N,N-diisopropyltryptamine (5-MeO-DIPT), a tryptamine-type designer drug, was studied using rat liver microsomal fractions and recombinant cytochrome P450 (CYP) enzymes. 5-MeO-DIPT was biotransformed mainly into a side-chain N-deisopropylated metabolite and partially into an aromatic ring O-demethylated metabolite in liver microsomal fractions from untreated rats of both sexes. This metabolic profile is different from our previous findings in human liver microsomal fractions, in which the aromatic ring O-demethylation was the major pathway whereas the side-chain N-deisopropylation was minor [Narimatsu S, Yonemoto R, Saito K, Takaya K, Kumamoto T, Ishikawa T, et al. oxidative metabolism of 5-methoxy-N,N-diisopropyltryptamine (Foxy) by human liver microsomes and recombinant cytochrome P450 enzymes. Biochem Pharmacol 2006;71:1377-85]. Kinetic and inhibition studies indicated that the side-chain N-dealkylation is mediated by CYP2C11 and CYP3A2, whereas the aromatic ring O-demethylation is mediated by CYP2D2 and CYP2C6 in untreated male rats. Pretreatment of male rats with p-naphthoflavone (BNF) produced an aromatic ring 6-hydroxylated metabolite. Recombinant rat and human CYP1A1 efficiently catalyzed 5-MeO-DIPT 6-hydroxylation under the conditions used. These results provide valuable information on the metabolic fate of 5-MeO-DIPT in rats that can be used in the toxicological study of this designer drug. (c) 2007 Elsevier Inc. All rights reserved.

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  • 小胞外過剰ドパミンによるドパミン神経障害における共通因子としてのキノン体生成 Invited Reviewed

    宮崎育子, 浅沼幹人, Diaz-Corrales FJ, 三好 耕, 小川紀雄

    岡山医学会雑誌   119 ( 1 )   235 - 239   2008.1

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  • Preventing effects of a novel anti-parkinsonian agent zonisamide on dopamine quinone formation Reviewed

    Masato Asanuma, Ikuko Miyazaki, Francisco J. Diaz-Corrales, Ko Miyoshi, Norio Ogawa, Miho Murata

    Neuroscience Research   60 ( 1 )   106 - 113   2008.1

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    The neurotoxicity of dopamine (DA) quinones as dopaminergic neuron-specific oxidative stress is considered to play a role in the pathogenesis and/or progression of Parkinson's disease (PD), since DA quinones conjugate with several key PD pathogenic molecules (e.g., tyrosine hydroxylase, alpha-synuclein and parkin) to form protein-bound quinone (quinoprotein) and consequently inhibit their functions. Zonisamide (ZNS) is used as an anti-epileptic agent but also improved the cardinal symptoms of PD in recent clinical trials in Japan. To evaluate the effects of ZNS on excess cytosolic free DA-induced quinone toxicity, we examined changes in DA quinone-related indices after ZNS treatment both in in vitro cell-free system and in cultured cells. Co-incubation of DA and ZNS in a cell-free system caused conversion of DA to stable melanin via formation of DA-semiquinone radicals and DA chrome. Long-term (5 days) treatment with ZNS decreased quinoprotein and increased DA/DOPA chromes in dopaminergic CATH.a cells. ZNS significantly inhibited quinoprotein formation induced by treatment with tetrahydrobiopterin and ketanserin that elevate cytosolic free DA in the cells. Our results suggest that the novel anti-parkinsonian agent ZNS possesses preventing effects against DA quinone formation induced by excess amount of cytosolic DA outside the synaptic vesicles. (c) 2007 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved.

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  • [New perspectives on the mechanism of methamphetamine-induced neurotoxicity] Reviewed

    28 ( 2 )   49 - 61   2008

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  • 食品容器および食器より溶出する化学物質のドパミン神経障害性に関する研究─ビスフェノールAの培養ドパミン神経系への作用─

    喜多大三, 竹島美香, 田中弓子, 宮崎育子, 浅沼幹人

    九州栄養福祉大学研究紀要   4   89 - 97   2007.12

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  • Protective effects of metallothionein against dopamine quinone-induced dopaminergic neurotoxicity Reviewed

    Ikuko Miyazaki, Masato Asanuma, Hiroaki Hozumi, Ko Miyoshi, Norio Sogawa

    FEBS Letters   581 ( 25 )   5003 - 5008   2007.10

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    Dopamine (DA) quinone as DA neuron-specific oxidative stress conjugates with cysteine residues in functional proteins to form quinoproteins. Here, we examined the effects of cysteine-rich metal-binding proteins, metallothionein (NIT)-1 and -2, on DA quinone-induced neurotoxicity. NIT quenched DA semiquinones in vitro. In dopaminergic cells, DA exposure increased quinoproteins and decreased cell viability; these were ameliorated by pretreatment with MT-inducer zinc. Repeated L-DOPA administration markedly elevated striatal quinoprotein levels and reduced the DA nerve terminals specifically on the lesioned side in NIT-knockout parkinsonian mice, but not in wild-type mice. Our results suggested that intrinsic NIT protects against L-DOPA-induced DA quinone neurotoxicity in parkinsonian mice by its quinone-quenching property. (c) 2007 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

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  • Common anti-inflammatory drugs are potentially therapeutic for Parkinson's disease? Invited Reviewed

    Masato Asanuma, Ikuko Miyazaki

    Experimental Neurology   206 ( 2 )   172 - 178   2007.8

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    DOI: 10.1016/j.expneurol.2007.05.006

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  • 5-Methoxy-N,N-diisopropyltryptamine (Foxy), a selective and high affinity inhibitor of serotonin transporter Reviewed

    C. Sogawa, N. Sogawa, J. Tagawa, A. Fujino, K. Ohyama, M. Asanuma, M. Funada, S. Kitayama

    Toxicology Letters   170 ( 1 )   75 - 82   2007.4

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    5-Methoxy-N,N-diisopropyltryptamine (5-MeO-DIPT) is a synthetic orally active hallucinogenic tryptamine derivative, known also as Foxy or Foxy methoxy. However, few studies have examined its effects in vitro. In the present study, we investigated the actions of 5-MeO-DIPT against monoamine neurotransmitter transporters, including the transporters for dopamine (DAT), norepinephrine (NET), and serotonin (SERT), using COS-7 cells heterologously expressing these transporters and rat brain synaptosomes. 5-MeO-DIPT specifically inhibited the uptake of [H-3]serotonin (5-HT) by the SERT-expressing COS-7 cells and rat striatal synaptosomes in a high affinity manner at concentrations similar to those for cocaine. The effect was reversible and competitive. 5-MeO-DIPT failed to stimulate reverse transport of [H-3]5-HT through SERT, while it prevented the releasing action of methamphetamine. 5-MeO-DIPT induced cell toxicity at high concentrations in COS-7 cells, and it was not influenced by the expression of SERT. These results demonstrated that 5-MeO-DIPT acts as a competitive SERT inhibitor and has an inability to cause reverse transport, underlying its serotonergic actions. (C) 2007 Elsevier Ireland Ltd. All rights reserved.

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  • Suppression of p53-activated gene, PAG608, attenuates methamphetamine-induced neurotoxicity Reviewed

    Masato Asanuma, Ikuko Miyazaki, Youichirou Higashi, Francisco J. Diaz-Corrales, Masako Shimizu, Ko Miyoshi, Norio Ogawa

    Neuroscience Letters   414 ( 3 )   263 - 267   2007.3

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    The p53-activated gene 608 (PAG608) is a proapoptotic gene activated and regulated by p53 expression in oxidative stress-induced apoptosis of neuronal cells. In this study, we determined the role of PAG608 in methamphetamine-induced neurotoxicity. Treatment of mouse dopaminergic CATH.a cells with 2 mM methamphetamine increased PAG608 expression at 3 h followed by increase in phosphorylated p53 expression. Transient transfection of PAG608 antisense cDNA or RNA interference using PAG608 small interfering RNA significantly attenuated the dose-dependent decrease in cell viability of CATH.a cells by methamphetamine (1-4 mM) exposure. In monoaminergic neuronal B65 cells, which contain serotonin rather than dopamine, methamphetamine-induced cell death was also significantly but partially protected by transient transfection of PAG608 antisense cDNA. Furthermore, cell death of PC 12 cells produced by methamphetamine (1-5 mM) was almost completely prevented by stable expression of PAG608 antisense cDNA, compared with significant reduction of cell viability in control PC12 cells. Our results showed that suppression of PAG608 using transient and stable transfection with PAG608 anti sense cDNA or small interfering RNA attenuates methamphetamine-induced death of various monoaminergic neuronal cells, suggesting that methamphetamine neurotoxicity in monoaminergic cells is related, at least in part, to induction of PAG608 expression. (c) 2006 Elsevier Ireland Ltd. All rights reserved.

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  • Characterization of pericentrin isoforms in vivo Reviewed

    Ko Miyoshi, Masato Asanuma, Ikuko Miyazaki, Shinsuke Matsuzaki, Masaya Tohyama, Norio Ogawa

    Biochemical and Biophysical Research Communications   351 ( 3 )   745 - 749   2006.12

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    Pericentrin was first identified as a mouse centrosomal protein and is now referred to as pericentrin A. A larger homologous protein in humans with a C-terminal calmodulin-binding domain was later identified as pericentrin B. Pericentrin has been shown to be one of the key components in ciliogenesis.. but in vivo pericentrin products have remained ambiguous. Here we characterized pericentrin isoforms in mice. Two pericentrin transcripts of 9.5 and 6.9 kb were recognized on the mouse tissue Northern blots, while a cRNA probe for a 5'-terminal sequence shared by pericentrin A and B failed to hybridize to the 6.9-kb message. Two pericentrin cDNAs were identified, which encoded pericentrin B and a novel isoform, pericentrin S, sharing with pericentrin B a C-terminal calmodulin-binding motif. Three pericentrin proteins of 360, 255, and 250 kDa revealed by immunoprecipitation analysis were thought to correspond to pericentrin B, pericentrin S, and an unknown N-terminal product. (c) 2006 Elsevier Inc. All rights reserved.

    DOI: 10.1016/j.bbrc.2006.10.101

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  • Involvement of STAT3 in bladder smooth muscle hypertrophy following bladder outlet obstruction Reviewed

    Osamu Fujita, Masato Asanuma, Teruhiko Yokoyama, Ikuko Miyazaki, Norio Ogawa, Hiromi Kumon

    Acta Medica Okayama   60 ( 6 )   299 - 309   2006.12

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    We examined the involvement of the signal transducer and activator of transcription 3 (STAT3) in bladder outlet obstruction (BOO)-induced bladder smooth muscle hypertrophy using a rat in vivo and in vitro study. BOO induced increases in bladder weight and bladder smooth muscle thickness I week after the operation. By using antibody microarrays, 64 of 389 proteins blotted on the array met our selection criteria of an INR value between &gt;= 2.0 and &lt;= 0.5. This result revealed up-regulation of transcription factors, cell cycle regulatory proteins, apoptosis-associated proteins and so on. On the other hand, down-regulation (INR value &lt;= 0.5) of proteins was not found. In a profiling study, we found an increase in the expression of STAT3. A significant increase in nuclear phosphorylated STAT3 expression was confirmed in bladder smooth muscle tissue by immunohistochemistry and Western blot analysis. Cyclical stretch-relaxation (I Hz) at 120% elongation significantly increased the expression of STAT3 and of alpha-smooth muscle actin in primary cultured bladder smooth muscle cells. Furthermore, the blockade of STAT3 expression by the transfection of STAT3 small interfering RNA (siRNA) significantly prevented the stretch-induced increase in alpha-smooth muscle actin expression. These results suggest that STAT3 has an important role in the induction of bladder smooth muscle hypertrophy.

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  • Molecular basis of 6-hydroxydopamine-induced caspase activations due to increases in oxidative stress in the mouse striatum Reviewed

    Ken-ichi Tanaka, Norio Ogawa, Masato Asanuma

    Neuroscience Letters   410 ( 2 )   85 - 89   2006.12

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    To clarify the possible role of in the in vivo toxic effects of 6-hydroxydopamine (6-OHDA), especially caspase activations, we examined its effects on striatal lipid peroxidation (LPO) and caspase activations in 6-OHDA-lesioned mice. Both dopamine (DA) levels and DA turnover were significantly changed by the 6-OHDA i.c.v. injection compared with the pre-injection level in the striatum. In addition, the striatal glutathione (GSH) content fluctuated and was significantly decreased both at 3 and 14 days after 6-OHDA i.e.v. injection. Moreover, superoxide dismutase (SOD) activity at 7 days after 6-OHDA i.c.v. injection was transiently and significantly increased compared with the pre-injection level. The levels of thiobarbituric acid-reactive substances (TBA-RS) were significantly increased at 1, 3 and 14 days. 6-OHDA significantly increased the activities of all three caspases, except for the caspase-3 activity at 7 days throughout the experimental period compared with the pre-injection level. In conclusion, 6-OHDA-induced dopaminergic dysfunction is mainly due to caspase activations by increases in oxidative stress in the mouse striatum. (c) 2006 Elsevier Ireland Ltd. All rights reserved.

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  • Nonsteroidal anti-inflammatory drugs in Parkinson's disease: possible involvement of quinone formation Reviewed

    Masato Asanuma, Ikuko Miyazaki

    Expert Review of Neurotherapeutics   6 ( 9 )   1313 - 1325   2006.9

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    It has been revealed that nonsteroidal anti-inflammatory drugs (NSAIDs) have neuroprotective properties based not only on their cyclooxygenase-inhibitory action, but also on other properties including their inhibitory effects on the synthesis of nitric oxide radicals and agonistic action for peroxisome proliferator-activated receptor gamma, in addition to some as yet unknown properties. Recently, a number of experimental and clinical studies have examined the neuroprotective effects of NSAIDs on the pathogenesis of several neurodegenerative diseases, including Parkinson's disease. In this article, various pharmacological effects of NSAIDs (except for their cyclooxygenase-inhibitory action) are reviewed, and possible neuroprotective effects of NSAIDs on Parkinson's disease are discussed. The neurotoxicity of dopamine quinones, or DOPA quinones, has recently received attention as a dopaminergic neuron-specific oxidative stress that is known to play a role in the pathogenesis of Parkinson's disease and neurotoxin-induced parkinsonism. NSAIDs inhibit prostaglandin H synthase, thus suppressing dopamine oxidation and subsequent dopamine quinone formation. Therefore, this article also reviews possible suppressive effects of some NSAIDs against dopamine quinone generation. Expert Rev. Neurotherapeutics 6(9), 1313-1325 (2006)

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  • Embryonic expression of pericentrin suggests universal roles in ciliogenesis Reviewed

    Ko Miyoshi, Kazunari Onishi, Masato Asanuma, Ikuko Miyazaki, Francisco J. Diaz-Corrales, Norio Ogawa

    Development Genes and Evolution   216 ( 9 )   537 - 542   2006.9

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    Pericentrin (Pcnt) is a giant coiled-coil protein known to mediate microtubule organization. It has been recently reported that mitosis-specific centrosomal anchoring of gamma tubulin complexes by Pcnt acts to control mitotic spindle organization, though little is known about the in vivo expression of Pcnt. In this study, we investigated Pcnt expression in mouse embryos. In situ hybridization analysis revealed preferential expression of Pcnt in quiescent G(0) phase cells throughout the embryo with an unexpectedly low expression level in proliferating cells, suggesting that Pcnt might not play an important role in mitotic proliferation. Immunofluorescence analysis confirmed preferential expression of the Pcnt protein in G(0) phase cells. Moreover, Pcnt was shown to be localized to the base of primary cilia in multiple embryonic tissues, in agreement with a recent study demonstrating the involvement of Pcnt in primary cilia formation using cultured mammalian cells.

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  • Oxidative metabolism of 5-methoxy-N,N-diisopropyltryptamine (Foxy) by human liver microsomes and recombinant cytochrome P450 enzymes Reviewed

    Shizuo Narimatsu, Rei Yonemoto, Keita Saito, Kazuo Takaya, Takuya Kumamoto, Tsutomu Ishikawa, Masato Asanuma, Masahiko Funada, Kimio Kiryu, Shinsaku Naito, Yuzo Yoshida, Shigeo Yamamoto, Nobumitsu Hanioka

    Biochemical Pharmacology   71 ( 9 )   1377 - 1385   2006.4

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    DOI: 10.1016/j.bcp.2006.01.015

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  • Centrosome overduplication induced by rotenone treatment affects the cellular distribution of p53 tumor suppressor protein in the neuroblastoma B65 cell line

    Francisco J Diaz-Corrales, Masato Asanuma, Ikuko Miyazaki, Ko Miyoshi, Norio Ogawa

    Psychiatry and Clinical Neurosciences   60   S18 - S26   2006.4

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  • Methamphetamine‐induced dopaminergic neurotoxicity is regulated by quinone formation‐related molecules Reviewed

    Ikuko Miyazaki, Masato Asanuma, Francisco J. Diaz‐Corrales, Masaya Fukuda, Kiyoyuki Kitaichi, Ko Miyoshi, Norio Ogawa

    The FASEB Journal   20 ( 3 )   571 - 573   2006.3

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    DOI: 10.1096/fj.05-4996fje

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  • 腹膜透析におけるラジカル分子特異的測定と腹膜硬化症早期診断マーカーの確立.

    杉山 斉, 菊本陽子, 浅沼幹人, 平松 信, 槇野博史

    腎臓   29 ( 2 )   112 - 117   2006

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  • ドパミン受容体アゴニストによるドパミンニューロン死の制御. Invited

    浅沼幹人

    Clinical Neuroscience   23 ( 12 )   1342 - 1343   2005.12

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  • 酸化ストレスによる神経障害と神経保護療法─ドパミン神経特異的酸化ストレスとしてのキノン体毒性. Invited

    浅沼幹人, 小川紀雄

    医学のあゆみ   215 ( 10 )   785 - 792   2005.12

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  • L-DOPA treatment from the viewpoint of neuroprotection Reviewed

    Norio Ogawa, Masato Asanuma, Ikuko Miyazaki, Francisco J. Diaz-Corrales, Ko Miyoshi

    Journal of Neurology   252 ( S4 )   iv23 - iv31   2005.10

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    DOI: 10.1007/s00415-005-4006-7

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  • Prednisolone Inhibits Proliferation of Cultured Pulmonary Artery Smooth Muscle Cells of Patients With Idiopathic Pulmonary Arterial Hypertension Reviewed

    Aiko Ogawa, Kazufumi Nakamura, Hiromi Matsubara, Hideki Fujio, Tetsuya Ikeda, Kaoru Kobayashi, Ikuko Miyazaki, Masato Asanuma, Katsumasa Miyaji, Daiji Miura, Kengo Fukushima Kusano, Hiroshi Date, Tohru Ohe

    Circulation   112 ( 12 )   1806 - 1812   2005.9

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    <bold>
    <italic>Background—</italic>
    </bold>
    Idiopathic pulmonary arterial hypertension (IPAH) is associated with proliferation of smooth muscle cells (SMCs) in small pulmonary arteries. There is no therapy that specifically inhibits SMC proliferation. Recent studies reported that prednisolone (PSL) inhibits the postangioplasty proliferation of SMCs in atherosclerotic arteries. In this study, we tested the hypothesis that PSL has antiproliferative effects on pulmonary artery SMCs of patients with IPAH.




    <bold>
    <italic>Methods and Results—</italic>
    </bold>
    Pulmonary artery SMCs were harvested from the pulmonary arteries of 6 patients with IPAH who underwent lung transplantation. Control SMCs were obtained from 5 patients with bronchogenic carcinoma who underwent lung lobectomy. After incubation in the presence of platelet-derived growth factor (PDGF), PSL was added at different concentrations and cell proliferation was assessed by
    3
    H-thymidine incorporation. PSL (2×10
    −4
    and 2×10
    −3
    mol/L) significantly inhibited PDGF-stimulated proliferation (
    <italic>P</italic>
    &lt;0.05) of SMCs from patients with IPAH but did not affect cell viability of SMCs, as confirmed by trypan blue staining. In cell cycle analysis using a microscope-based multiparameter laser scanning cytometer, PSL inhibited the progression of SMCs from G
    0
    /G
    1
    to the S phase. This inhibition was associated with increased p27 expression level. PSL (2×10
    −4
    mol/L) also inhibited PDGF-induced SMC migration.




    <bold>
    <italic>Conclusions—</italic>
    </bold>
    Our results indicate that PSL has an antiproliferative effect on cultured SMCs of pulmonary arteries from patients with IPAH and suggest that PSL may be potentially useful therapeutically in patients with IPAH.

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  • Dopamine agonist pergolide prevents levodopa-induced quinoprotein formation in Parkinsonian striatum and shows quenching effects on dopamine-semiquinone generated in vitro Reviewed

    Ikuko Miyazaki, Masato Asanuma, Francisco J. Diaz-Corrales, Ko Miyoshi, Norio Ogawa

    Clinical Neuropharmacology   28 ( 4 )   155 - 160   2005.7

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    The neurotoxicity of dopamine (DA) quinones that appears in dopaminergic neuron-specific oxidative stress has recently been shown to play a role in the pathogenesis and/or progression of Parkinson disease. To clarify the effects of a DA agonist, pergolide, on the levodopa-induced elevation of quinones, the authors examined, striatal changes in quinoprotein using a hemi-parkinsonian mouse model. The level of striatal quinoprotein was significantly elevated specifically on the parkinsonian side, but not on the control side, after repeated levodopa administration. This levodopa-induced increase in striatal quinoprotein was almost completely suppressed by adjunctive administration with pergolide on the lesioned side. Furthermore, it was clarified that pergolide scavenged DA-semiquinones generated in vitro in a dose-dependent manner. These suppressive and quenching effects of pergolide against cytotoxic DA quinones may play a key role in its neuroprotective mechanism in the parkinsonian brain. Copyright © 2005 by Lippincott Williams &amp
    Wilkins.

    DOI: 10.1097/01.wnf.0000175523.33334.24

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  • 薬物依存・毒性発現にかかわる分子の分子生物学的検索法─網羅的プロファイリングを中心に. Invited

    浅沼幹人, 宮崎育子

    日本薬理学雑誌   126 ( 1 )   30 - 34   2005.7

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    DOI: 10.1254/fpj.126.30

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  • Pramipexole has ameliorating effects on levodopa-induced abnormal dopamine turnover in parkinsonian striatum and quenching effects on dopamine-semiquinone generatedin vitro Reviewed

    Masato Asanuma, Ikuko Miyazaki, Francisco J. Diaz-Corrales, Masako Shimizu, Ken-ichi Tanaka, Norio Ogawa

    Neurological Research   27 ( 5 )   533 - 539   2005.7

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    DOI: 10.1179/016164105x22093

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  • Common anti-apoptotic roles of parkin and α-synuclein in human dopaminergic cells Reviewed

    Yutaka Machida, Tomoki Chiba, Atsushi Takayanagi, Yoshikazu Tanaka, Masato Asanuma, Norio Ogawa, Akihiko Koyama, Takeshi Iwatsubo, Shosuke Ito, Poul Hening Jansen, Nobuyoshi Shimizu, Keiji Tanaka, Yoshikuni Mizuno, Nobutaka Hattori

    Biochemical and Biophysical Research Communications   332 ( 1 )   233 - 240   2005.6

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    DOI: 10.1016/j.bbrc.2005.04.124

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  • Rotenone induces aggregation of γ-tubulin protein and subsequent disorganization of the centrosome: Relevance to formation of inclusion bodies and neurodegeneration Reviewed

    Francisco J. Diaz-Corrales, Masato Asanuma, Ikuko Miyazaki, Ko Miyoshi, Norio Ogawa

    Neuroscience   133 ( 1 )   117 - 135   2005.1

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    DOI: 10.1016/j.neuroscience.2005.01.044

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  • Direct evidence for expression of dopamine receptors in astrocytes from basal ganglia Reviewed

    Ikuko Miyazaki, Masato Asanuma, Francisco J. Diaz-Corrales, Ko Miyoshi, Norio Ogawa

    Brain Research   1029 ( 1 )   120 - 123   2004.12

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    Expression of dopamine receptors (DA-Rs) in astrocytes was examined in vitro and in vivo using primary cultured astrocytes and brain slices from rat basal ganglia. Astrocytes from basal ganglia expressed DA D1-, D3-, D4- and D5-receptors and D4-mediated signal transduction in response to DA, suggesting possible involvement of astrocytes in the pharmacological action of atypical antipsychotic drugs and in DA response in some neurological diseases. © 2004 Elsevier B.V. All rights reserved.

    DOI: 10.1016/j.brainres.2004.09.014

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  • Quinone formation as dopaminergic neuron-specific oxidative stress in the pathogenesis of sporadic Parkinson's disease and neurotoxin-induced parkinsonism.

    Masato Asanuma, Ikuko Miyazaki, Francisco J Diaz-Corrales, Norio Ogawa

    Acta Medica Okayama   58 ( 5 )   221 - 233   2004.10

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    DOI: 10.18926/AMO/32105

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  • Specific Gene Expression and Possible Involvement of Inflammation in Methamphetamine-Induced Neurotoxicity Reviewed

    Masato Asanuma, Ikuko Miyazaki, Youichirou Higashi, Takeshi Tsuji, Norio Ogawa

    Annals of the New York Academy of Sciences   1025 ( 1 )   69 - 75   2004.10

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    DOI: 10.1196/annals.1316.009

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  • パーキンソン病における細胞死の機序. Invited

    小川紀雄, 浅沼幹人, 三好 耕

    日本臨床   62 ( 9 )   1629 - 1634   2004.9

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  • Expression of metallothionein-III and cell death in differentiated catecholaminergic neuronal cells Reviewed

    Youichirou Higashi, Masato Asanuma, Ikuko Miyazaki, Norio Ogawa

    Neurological Research   26 ( 6 )   671 - 676   2004.9

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    DOI: 10.1179/016164104225015895

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  • Metallothioneins and neurodegenerative diseases Reviewed

    Isao Hozumi, Masato Asanuma, Mitsunori Yamada, Yoko Uchida

    Journal of Health Science   50 ( 4 )   323 - 331   2004.8

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    A symposium on the clinical aspects of metallothioneins (MTs) in neurodegenerative diseases was held at the 2003 Society of Metallothionein Meeting in Gifu, Japan. The objectives of the symposium were to review and speculate on the potential roles of MTs, especially MT-3 in neurodegenerative diseases such as Alzheimer's disease (AD), Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS) and spinocerebellar degeneration (SCD). Dr. Uchida discussed the controversial problem regarding the expression of MT-3 in AD brains. Dr. Asanuma addressed the function of MTs in the progression of PD and Dr. Hozumi described the therapeutic potential of MTs for ALS, while Dr. Yamada provided immunohistochemical findings of MT-3 in SCD for the first time. Although there are still controversial problems on MTs, this review provides proof that MTs are promising potential therapeutic targets for therapy for some neurodegenerative diseases.

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  • Molecular Basis of Anti-Apoptotic Effect of Immunophilin Ligands on Hydrogen Peroxide–Induced Apoptosis in Human Glioma Cells Reviewed

    Ken-ichi Tanaka, Masato Asanuma, Norio Ogawa

    Neurochemical Research   29 ( 8 )   1529 - 1536   2004.8

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    DOI: 10.1023/b:nere.0000029565.92587.25

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  • Parkin attenuates manganese‐induced dopaminergic cell death Reviewed

    Youichirou Higashi, Masato Asanuma, Ikuko Miyazaki, Nobutaka Hattori, Yoshikuni Mizuno, Norio Ogawa

    Journal of Neurochemistry   89 ( 6 )   1490 - 1497   2004.6

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    DOI: 10.1111/j.1471-4159.2004.02445.x

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  • DISC1 localizes to the centrosome by binding to kendrin Reviewed

    Ko Miyoshi, Masato Asanuma, Ikuko Miyazaki, Francisco J. Diaz-Corrales, Taiichi Katayama, Masaya Tohyama, Norio Ogawa

    Biochemical and Biophysical Research Communications   317 ( 4 )   1195 - 1199   2004.5

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    DOI: 10.1016/j.bbrc.2004.03.163

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  • 酸化ストレスとミトコンドリア機能障害,炎症反応.―孤発性パーキンソン病とドパミン神経毒研究から得たもの. Invited

    浅沼幹人

    内科   93 ( 4 )   611 - 615   2004.4

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  • Neuroprotective Effects of Nonsteroidal Anti-inflammatory Drugs on Neurodegenerative Diseases Reviewed

    M. Asanuma, I. Miyazaki, N. Ogawa

    Current Pharmaceutical Design   10 ( 6 )   695 - 700   2004.2

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    DOI: 10.2174/1381612043453072

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  • Parkinson病薬物治療の将来 ―進行抑制薬実現の可能性. Invited

    小川紀雄, 浅沼幹人, 田中健一

    医学のあゆみ   208 ( 6 )   583 - 588   2004.2

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  • 実験的パーキンソニズムに使われる薬剤.〜MPTP,6-ヒドロキシドパミンならびにロテノン〜. Invited

    浅沼幹人, 宮崎育子, 小川紀雄

    医薬ジャーナル   40 ( 1 )   111 - 116   2004.1

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  • Rotenone induces disassembly of the Golgi apparatus in the rat dopaminergic neuroblastoma B65 cell line Reviewed

    Francisco J. Diaz-Corrales, Masato Asanuma, Ikuko Miyazaki, Norio Ogawa

    Neuroscience Letters   354 ( 1 )   59 - 63   2004.1

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    DOI: 10.1016/j.neulet.2003.09.059

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  • 遺伝子改変によるパーキンソン病モデル. Invited

    浅沼幹人, 宮崎育子

    脳の科学   292 ( 2004年増刊号 )   165 - 170   2004

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  • β遮断薬による心不全・不整脈治療の基礎と臨床ーカルベジロールを中心としてーβ遮断薬と酸化ストレス. Reviewed

    中村一文, 垣下幹夫, 草野研吾, 三浦 綾, 久松研一, 永瀬 聡, 森田 宏, 斉藤博則, 江森哲郎, 浅沼幹人, 小川紀雄, 宮崎正博, 中村陽一, 松原広己, 伏見和郎, 豊國伸哉, 大江 透

    心電図   24 ( 1 )   15 - 21   2004

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    欧米における大規模臨床試験の結果は,β遮断薬が慢性心不全の生命予後改善のみならず,突然死も有意に抑制することを明らかにした.しかし,患者背景の異なる我が国における,β遮断薬の有効性は必ずしも明確ではない.そこで,著者等の自験例を基に,致死性不整脈患者或いは慢性心不全患者に対するカルベジロールを中心としたβ遮断薬の予後に対する影響及び突然死予防効果,その機序について検討した

    DOI: 10.5105/jse.24.15

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  • Direct Evidence for Increased Hydroxyl Radicals in Angiotensin II-induced Cardiac Hypertrophy through Angiotensin II Type 1a Receptor Reviewed

    Mikio Kakishita, Kazufumi Nakamura, Masato Asanuma, Hiroshi Morita, Hironori Saito, Kengo Kusano, Yoichi Nakamura, Tetsuro Emori, Hiromi Matsubara, Takeshi Sugaya, Norio Ogawa, Tohru Ohe

    Journal of Cardiovascular Pharmacology   42 ( Suppl 1 )   S67 - S70   2003.12

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    DOI: 10.1097/00005344-200312001-00015

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  • Methamphetamine-induced neurotoxicity in mouse brain is attenuated by ketoprofen, a non-steroidal anti-inflammatory drug Reviewed

    Masato Asanuma, Takeshi Tsuji, Ikuko Miyazaki, Ko Miyoshi, Norio Ogawa

    Neuroscience Letters   352 ( 1 )   13 - 16   2003.11

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  • ドパミンおよびその誘導体のキノン体生成を介したアポトーシス誘導性.

    浅沼幹人, 宮崎育子, Haque ME, 東 洋一郎, 小川紀雄

    Prog Med   23 ( 10 )   2736 - 2741   2003.10

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  • Overexpression of Cu–Zn superoxide dismutase protects neuroblastoma cells against dopamine cytotoxicity accompanied by increase in their glutathione level Reviewed

    M.Emdadul Haque, Masato Asanuma, Youichirou Higashi, Ikuko Miyazaki, Ken-ichi Tanaka, Norio Ogawa

    Neuroscience Research   47 ( 1 )   31 - 37   2003.9

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    DOI: 10.1016/s0168-0102(03)00166-4

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  • Dopamine- or L-DOPA-induced neurotoxicity: The role of dopamine quinone formation and tyrosinase in a model of Parkinson’s disease Reviewed

    Masato Asanuma, Ikuko Miyazaki, Norio Ogawa

    Neurotoxicity Research   5 ( 3 )   165 - 176   2003.1

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    DOI: 10.1007/bf03033137

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  • Apoptosis-inducing neurotoxicity of dopamine and its metabolites via reactive quinone generation in neuroblastoma cells Reviewed

    M Emdadul Haque, Masato Asanuma, Youichirou Higashi, Ikuko Miyazaki, Ken-ichi Tanaka, Norio Ogawa

    Biochimica et Biophysica Acta - General Subjects   1619 ( 1 )   39 - 52   2003.1

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    DOI: 10.1016/s0304-4165(02)00440-3

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  • 非ステロイド性消炎鎮痛薬の神経保護作用の新展開. Reviewed

    浅沼幹人, 宮崎育子, 辻 武史, 小川紀雄

    日本神経精神薬理学会雑誌   23 ( 3 )   111 - 119   2003

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  • アルツハイマー病脳で減少しているgrowth inhibitory factor (GIF) の加齢にともなう変化.

    浅沼幹人, 宮崎育子, 東 洋一郎, 田中健一, 小川紀雄

    分子精神医学   3 ( 1 )   69 - 70   2003

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  • テトラサイクリン誘導体ミノサイクリンの種々の神経障害に対する保護作用. Invited

    浅沼幹人

    ファルマシア   38 ( 11 )   1105 - 1106   2002.11

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  • The p53-activated Gene, PAG608, Requires a Zinc Finger Domain for Nuclear Localization and Oxidative Stress-induced Apoptosis Reviewed

    Youichirou Higashi, Masato Asanuma, Ikuko Miyazaki, M. Emdadul Haque, Naoko Fujita, Ken-ichi Tanaka, Norio Ogawa

    Journal of Biological Chemistry   277 ( 44 )   42224 - 42232   2002.11

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    DOI: 10.1074/jbc.m203594200

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  • Age-related changes in expression of metallothionein-III in rat brain Reviewed

    Ikuko Miyazaki, Masato Asanuma, Youichirou Higashi, Chiharu Aoki Sogawa, Ken-ichi Tanaka, Norio Ogawa

    Neuroscience Research   43 ( 4 )   323 - 333   2002.8

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    DOI: 10.1016/s0168-0102(02)00057-3

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  • The dopamine agonist cabergoline provides neuroprotection by activation of the glutathione system and scavenging free radicals Reviewed

    Michiyo Yoshioka, Ken-ichi Tanaka, Ikuko Miyazaki, Naoko Fujita, Youichirou Higashi, Masato Asanuma, Norio Ogawa

    Neuroscience Research   43 ( 3 )   259 - 267   2002.7

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    DOI: 10.1016/s0168-0102(02)00040-8

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  • Aggravation of 6-hydroxydopamine-induced dopaminergic lesions in metallothionein-I and -II knock-out mouse brain Reviewed

    Masato Asanuma, Ikuko Miyazaki, Youichirou Higashi, Ken-ichi Tanaka, Md Emdadul Haque, Naoko Fujita, Norio Ogawa

    Neuroscience Letters   327 ( 1 )   61 - 65   2002.7

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    DOI: 10.1016/s0304-3940(02)00346-4

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  • Methamphetamine-induced increase in striatal p53 DNA-binding activity is attenuated in Cu,Zn-superoxide dismutase transgenic mice Reviewed

    Masato Asanuma, Ikuko Miyazaki, Youichirou Higashi, Jean Lud Cadet, Norio Ogawa

    Neuroscience Letters   325 ( 3 )   191 - 194   2002.6

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    DOI: 10.1016/s0304-3940(02)00291-4

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  • ニューロメラニン合成酵素チロシナーゼのドパミン神経障害への関与.

    浅沼幹人, 東 洋一郎, 宮崎育子, 小川紀雄

    Prog Med   22 ( 1 )   212 - 215   2002.1

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  • Progressive cortical atrophy after forebrain ischemia in diabetic rats Reviewed

    Fumio Kondo, Masato Asanuma, Ikuko Miyazaki, Yoichi Kondo, Ken-ichi Tanaka, Hirohumi Makino, Norio Ogawa

    Neuroscience Research   39 ( 3 )   339 - 346   2001.3

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    DOI: 10.1016/s0168-0102(00)00233-9

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  • Neuroprotective effects of non-steroidal anti-inflammatory drugs by direct scavenging of nitric oxide radicals Reviewed

    Masato Asanuma, Sakiko Nishibayashi-Asanuma, Ikuko Miyazaki, Masahiro Kohno, Norio Ogawa

    Journal of Neurochemistry   76 ( 6 )   1895 - 1904   2001.3

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    DOI: 10.1046/j.1471-4159.2001.00205.x

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  • Delta opioid peptide [D-Ala2, D-Leu5]enkephalin causes a near complete blockade of the neuronal damage induced by a single high dose of methamphetamine: Examining the role of p53 Reviewed

    Teruo Hayashi, Hiroshi Hirata, Masato Asanuma, Bruce Ladenheim, Li-I Tsao, Jean Lud Cadet, Tsung-Ping Su

    Synapse   39 ( 4 )   305 - 312   2001.3

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    DOI: 10.1002/1098-2396(20010315)39:4<305::aid-syn1013>3.0.co;2-e

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  • Localization, regulation, and function of metallothionein-III/growth inhibitory factor in the brain. Reviewed

    Chiharu Aoki Sogawa, Masato Asanuma, Norio Sogawa, Ikuko Miyazaki, Tohru Nakanishi, Hiroaki Furuta, Norio Ogawa

    Acta Medica Okayama   55 ( 1 )   1 - 9   2001.2

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    DOI: 10.18926/AMO/32031

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  • 酸化ストレスと神経細胞死. Invited

    小川紀雄, 浅沼幹人

    Clinical Neuroscience   19 ( 6 )   665 - 667   2001

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  • フリーラジカルと脳障害. Invited

    浅沼幹人, 小川紀雄

    Clinical Neuroscience   19 ( 5 )   555 - 559   2001

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  • Molecular mechanism in activation of glutathione system by ropinirole, a selective dopamine D2 agonist. Reviewed

    Ken-ichi Tanaka, Ikuko Miyazaki, Naoko Fujita, Md Emdadul Haque, Masato Asanuma, Norio Ogawa

    Neurochemical Research   26 ( 1 )   31 - 36   2001

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    DOI: 10.1023/a:1007672414239

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  • Immunophilin ligands prevent H2O2-induced apoptotic cell death by increasing glutathione levels in neuro 2A neuroblastoma cells. Reviewed

    Ken-ichi Tanaka, Naoko Fujita, Masato Asanuma, Norio Ogawa

    Acta Medica Okayama   54 ( 6 )   275 - 280   2000.12

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:Okayama University Medical School  

    DOI: 10.18926/AMO/32278

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  • Expression of metallothionein-III mRNA and its regulation by levodopa in the basal ganglia of hemi-parkinsonian rats Reviewed

    Ikuko Miyazaki, Chiharu Aoki Sogawa, Masato Asanuma, Youichirou Higashi, Ken-ichi Tanaka, Tohru Nakanishi, Norio Ogawa

    Neuroscience Letters   293 ( 1 )   65 - 68   2000.10

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    DOI: 10.1016/s0304-3940(00)01488-9

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  • Inhibition of Tyrosinase Reduces Cell Viability in Catecholaminergic Neuronal Cells Reviewed

    Youichirou Higashi, Masato Asanuma, Ikuko Miyazaki, Norio Ogawa

    Journal of Neurochemistry   75 ( 4 )   1771 - 1774   2000.10

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    DOI: 10.1046/j.1471-4159.2000.0751771.x

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  • Direct interactions of methamphetamine with the nucleus Reviewed

    Masato Asanuma, Teruo Hayashi, Sonia V Ordonèz, Norio Ogawa, Jean Lud Cadet

    Molecular Brain Research   80 ( 2 )   237 - 243   2000.9

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    DOI: 10.1016/s0169-328x(00)00128-5

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  • Bromocriptine markedly suppress levodopa-induced abnormal increase of dopamine turnover in the parkinsonian striatum Reviewed

    Norio Ogawa, Ken-ichi Tanaka, Masato Asanuma

    Neurochemical Research   25 ( 6 )   755 - 758   2000.6

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    DOI: 10.1023/a:1007530720544

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  • フリーラジカルと神経細胞死. Invited

    浅沼幹人, 小川紀雄

    Clinical Neuroscience   18 ( 4 )   415 - 417   2000.4

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  • Antioxidants protect against dopamine-induced metallothionein-III (GIF) mRNA expression in mouse glial cell line (VR-2g) Reviewed

    Chiharu Aoki Sogawa, Ikuko Miyazaki, Norio Sogawa, Masato Asanuma, Norio Ogawa, Hiroaki Furuta

    Brain Research   853 ( 2 )   310 - 316   2000.1

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    DOI: 10.1016/s0006-8993(99)02284-2

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  • Protective effect of oren-gedoku-to against induction of neuronal death by transient cerebral ischemia in the C57BL/6 mouse Reviewed

    Yoichi Kondo, Fumio Kondo, Masato Asanuma, Ken-ichi Tanaka, Norio Ogawa

    Neurochemical Research   25 ( 2 )   205 - 209   2000

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    DOI: 10.1023/a:1007515318434

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  • Bifemelane hydrochloride protects against cytotoxicity of hydrogen peroxide on cultured rat neuroblastoma cell line Reviewed

    Ikuko Miyazaki, Emi Iwata-Ichikawa, Masato Asanuma, Motoyuki Iida, Norio Ogawa

    Neurochemical Research   24 ( 7 )   857 - 860   1999.7

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    DOI: 10.1023/a:1020953913490

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  • Glial Cells Protect Neurons Against Oxidative Stress via Transcriptional Up-Regulation of the Glutathione Synthesis Reviewed

    Emi Iwata-Ichikawa, Yoichi Kondo, Ikuko Miyazaki, Masato Asanuma, Norio Ogawa

    Journal of Neurochemistry   72 ( 6 )   2334 - 2344   1999.6

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    DOI: 10.1046/j.1471-4159.1999.0722334.x

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  • Nitric oxide modulates muscarinic acetylcholine receptor binding in the cerebral cortex of gerbils Reviewed

    Marvin Gómez-Vargas, Masato Asanuma, Sakiko Nishibayashi-Asanuma, Emi Iwata, Norio Ogawa

    Neurochemical Research   24 ( 5 )   629 - 635   1999.5

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    DOI: 10.1023/a:1021044107323

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  • パーキンソン病と活性酸素・窒素種. Invited

    浅沼幹人, 小川紀雄

    神経研究の進歩   43 ( 2 )   264 - 274   1999.4

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    DOI: 10.11477/mf.1431901046

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  • Early treatment with cyclosporin A ameliorates the reduction of muscarinic acetylcholine receptors in gerbil hippocampus after transient forebrain ischemia Reviewed

    Yoichi Kondo, Masato Asanuma, Emi Iwata, Fumio Kondo, Ikuko Miyazaki, Norio Ogawa

    Neurochemical Research   24 ( 1 )   9 - 13   1999

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    DOI: 10.1023/a:1020915727119

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  • Neural transplantation normalizes dopaminegic dysfunction in an animal model of Parkinson's disease. Reviewed

    Norio Ogawa, Kiminao Mizukawa, Hitoo Nishino, Masato Asanuma, Mitsutoshi Yamamoto

    Journal of Brain Science   25 ( 3-4 )   133 - 138   1999

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  • ホスホジエステラーゼ Invited

    浅沼幹人

    生体の科学   49 ( 5 )   499 - 501   1998.10

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    DOI: 10.11477/mf.2425901650

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  • Chronic cerebral hypoperfusion disrupts discriminative behavior in acquired-learning rats Reviewed

    Ken-ichi Tanaka, Naoko Wada, Koji Hori, Masato Asanuma, Masahiko Nomura, Norio Ogawa

    Journal of Neuroscience Methods   84 ( 1-2 )   63 - 68   1998.10

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    DOI: 10.1016/s0165-0270(98)00092-2

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  • Melatonin attenuates methamphetamine-induced toxic effects on dopamine and serotonin terminals in mouse brain Reviewed

    Hiroshi Hirata, Masato Asanuma, Jean Lud Cadet

    Synapse   30 ( 2 )   150 - 155   1998.10

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    DOI: 10.1002/(sici)1098-2396(199810)30:2<150::aid-syn4>3.0.co;2-b

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  • Methamphetamine-induced increase in striatal NF-κB DNA-binding activity is attenuated in superoxide dismutase transgenic mice Reviewed

    Masato Asanuma, Jean Lud Cadet

    Molecular Brain Research   60 ( 2 )   305 - 309   1998.10

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    DOI: 10.1016/s0169-328x(98)00188-0

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  • Parkinson病とNO. Invited

    小川紀雄, 浅沼幹人

    Clinical Neuroscience   16 ( 7 )   806 - 808   1998.7

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  • Superoxide radicals are mediators of the effects of methamphetamine on Zif268 (Egr-1, NGFI-A) in the brain: evidence from using CuZn superoxide dismutase transgenic mice Reviewed

    Hiroshi Hirata, Masato Asanuma, Jean Lud Cadet

    Molecular Brain Research   58 ( 1-2 )   209 - 216   1998.7

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    DOI: 10.1016/s0169-328x(98)00055-2

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  • Protective effects of nicergoline against hydrogen peroxide toxicity in rat neuronal cell line Reviewed

    Emi Iwata, Ikuko Miyazaki, Masato Asanuma, Azusa Iida, Norio Ogawa

    Neuroscience Letters   251 ( 1 )   49 - 52   1998.7

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    DOI: 10.1016/s0304-3940(98)00489-3

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  • Pergolide scavenges both hydroxyl and nitric oxide free radicals in vitro and inhibits lipid peroxidation in different regions of the rat brain Reviewed

    Marvin Gómez-Vargas, Sakiko Nishibayashi-Asanuma, Masato Asanuma, Yoichi Kondo, Emi Iwata, Norio Ogawa

    Brain Research   790 ( 1-2 )   202 - 208   1998.4

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    DOI: 10.1016/s0006-8993(97)01521-7

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  • Attenuation of 6-hydroxydopamine-induced dopaminergic nigrostriatal lesions in superoxide dismutase transgenic mice Reviewed

    Masato Asanuma, Hiroshi Hirata, Jean L Cadet

    Neuroscience   85 ( 3 )   907 - 917   1998.4

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    DOI: 10.1016/s0306-4522(97)00665-9

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  • Manda, a fermented natural food, suppresses lipid peroxidation in the senescent rat brain Reviewed

    Motoko Kawai, Shingoro Matsuura, Masato Asanuma, Norio Ogawa

    Neurochemical Research   23 ( 4 )   455 - 461   1998.4

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    DOI: 10.1023/a:1022475830587

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  • Effects of repeated cyclosporin A administration on iminodipropionitrile-induced dyskinesia and TRE-/CRE-binding activities in rat brain Reviewed

    Kyoko Iida, Emi Iwata, Masato Asanuma, Sakiko N Asanuma, Marvin Gómez-Vargas, Ikuko Miyazaki, Tohru Nakanishi, Norio Ogawa

    Neuroscience Research   30 ( 2 )   185 - 193   1998.2

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    DOI: 10.1016/s0168-0102(97)00128-4

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  • Effects of Lecithinized SOD on Sequential Change in SOD Activity after Cerebral Contusion in Rats Reviewed

    Masatoshi Yunoki, Masamitsu Kawauchi, Naoya Ukita, Yasuhiro Noguchi, Shinsaku Nishio, Yasuhiro Ono, Shoji Asari, Takashi Ohmoto, Masato Asanuma, Norio Ogawa

    Acta Neurochir Suppl   71   142 - 145   1998

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    DOI: 10.1007/978-3-7091-6475-4_42

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  • Dantrolene sodium reverses the increase in cAMP response element and TPA responsive element DNA-binding activity in the rabbit brain following haloperidol administration and heat stress Reviewed

    Hisashi Tanii, Norio Taniguchi, Ichiro Tsujio, Masato Asanuma, Emi Iwata, Takashi Kudo, Norio Ogawa, Masatoshi Takeda

    Psychiatry and Clinical Neurosciences   51 ( 6 )   415 - 420   1997.12

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    DOI: 10.1111/j.1440-1819.1997.tb02610.x

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  • Effects of Lecithinized Superoxide Dismutase on Traumatic Brain Injury in Rats Reviewed

    Masatoshi Yunoki, Masamitsu Kawauchi, Naoya Ukita, Yasuhiro Noguchi, Shinsaku Nishio, Yasuhiro Ono, Shoji Asari, Takashi Ohmoto, Masato Asanuma, Norio Ogawa

    Journal of Neurotrauma   14 ( 10 )   739 - 746   1997.10

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    DOI: 10.1089/neu.1997.14.739

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  • Different effects of oxidative stress on activation of transcription factors in primary cultured rat neuronal and glial cells Reviewed

    Emi Iwata, Masato Asanuma, Sakiko Nishibayashi, Yoichi Kondo, Norio Ogawa

    Molecular Brain Research   50 ( 1-2 )   213 - 220   1997.10

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    DOI: 10.1016/s0169-328x(97)00190-3

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  • Late-onset lipid peroxidation and neuronal cell death following transient forebrain ischemia in rat brain Reviewed

    Yoichi Kondo, Masato Asanuma, Sakiko Nishibayashi, Emi Iwata, Norio Ogawa

    Brain Research   772 ( 1-2 )   37 - 44   1997.10

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    DOI: 10.1016/s0006-8993(97)00836-6

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  • Genetic association between susceptibility to Parkinson's disease and α1-antichymotrypsin polymorphism Reviewed

    Mitsutoshi Yamamoto, Ikuko Kondo, Norio Ogawa, Masato Asanuma, Yoshiaki Yamashita, Yoshikuni Mizuno

    Brain Research   759 ( 1 )   153 - 155   1997.6

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    DOI: 10.1016/s0006-8993(97)00330-2

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  • Thyrotropin releasing hormone prevents abnormalities of cortical acetylcholine and monoamines in mice following head injury Reviewed

    Ken-ichi Tanakaa, Norio Ogawa, Masato Asanuma, Yoichi Kondo

    Regulatory Peptides   70 ( 2-3 )   173 - 178   1997.6

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    DOI: 10.1016/s0167-0115(97)01013-6

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  • Direct evidence of high DNA binding activity of transcription factor AP-1 in rheumatoid arthritis synovium Reviewed

    Hiroshi Asahara, Koushi Fujisawa, Tetsuji Kobata, Tomoko Hasunuma, Toshiro Maeda, Masato Asanuma, Norio Ogawa, Hajime Inoue, Takayuki Sumida, Kusuki Nishioka

    Arthritis & Rheumatism   40 ( 5 )   912 - 918   1997.5

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    DOI: 10.1002/art.1780400520

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  • Ketoprofen, a non-steroidal anti-inflammatory drug prevents the late-onset reduction of muscarinic receptors in gerbil hippocampus after transient forebrain ischemia Reviewed

    Masato Asanuma, Sakiko N Asanuma, Marvin Gómez-Vargas, Mitsutoshi Yamamoto, Norio Ogawa

    Neuroscience Letters   225 ( 2 )   109 - 112   1997.4

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    DOI: 10.1016/s0304-3940(97)00204-8

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  • 脳内転写制御因子CREB, AP-1のDNA結合活性に及ぼすドパミンレセプター作用薬の影響.

    浅沼幹人

    Prog. Med.   17 ( 2 )   423 - 430   1997.2

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  • 神経細胞死と活性酸素・フリーラジカル.. Invited

    小川紀雄, 近藤洋一, 岩田恵美, 浅沼幹人, 飯田基之

    フリーラジカルの臨床   11   101 - 106   1997

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  • Protective effects of FK506 on the late-onset reduction of muscarinic acetylcholine receptors in gerbil hippocampus after transient forebrain ischemia Reviewed

    Sakiko Nishibayashi, Yoichi Kondo, Masato Asanuma, Emi Iwata, Marvin Gomez-Vargas, Norio Ogawa

    Journal of Brain Science   23 ( 1 )   33 - 40   1997

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    Late-onset reduction of muscarinic acetylcholine receptors (LORMAR) in the ischemic gerbil hippocampus begins as late as 7 days after a 5-min transient forebrain ischemia and reperfusion. We previously reported that LORMAR is prevented by postadministration of cyclosporin A. In the present study, we aim to elucidate whether the LORMAR can also be prevented by post-ischemic administration of the immunosuppressant FK506 (tacrolimus). We investigated changes in muscarinic acetylcholine receptor binding capacity and histological examination in the transient forebrain ischemic gerbil hippocampus and the effect of this agent on these changes. In the ischemic vehicle-treated group, muscarinic acetylcholine receptors significantly decreased in the hippocampus as the LORMAR with subsequent disruption of the pyramidal cells in the CA1 area. On the other hand, LORMAR is prevented by daily subcutaneous administration of low dose of FK506 (0.5 mg/kg/day) for 10 days after the ischemic insult, although delayed neuronal cell death was not prevented. Thus, we showed that the LORMAR is attenuated by post-administration of FK506.

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  • Chronic administration of Oren-gedoku-to (TJ15) inhibits ischemic-induced changes in brain indoleamine metabolism and muscarinic receptor binding in the Mongolian gerbil Reviewed

    Hideaki Kabuto, Masato Asanuma, Sakiko Nishibayashi, Motoyuki Iida, Norio Ogawa

    Neurochemical Research   22 ( 1 )   33 - 36   1997

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    DOI: 10.1023/a:1027369119224

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  • Aniracetam ameriorates impaired pre- and post-synaptic cholinergic indices in gerbil hippocampus induced by transient forebrain ischemia Reviewed

    Yoichi Kondo, Masato Asanuma, Hideaki Kabuto, Emi Iwata, Fumio Kondo, Ikuko Miyazaki, Norio Ogawa

    Journal of Brain Science   23 ( 4 )   250 - 260   1997

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  • Effects of Lecithinized SOD on Contusion Injury in Rats Reviewed

    Masatoshi Yunoki, Yasuhiro Noguchi, Shinsaku Nishio, Yasuhiro Ono, Masamitsu Kawauchi, Shoji Asai, Takashi Ohmoto, Masato Asanuma, Norio Ogawa

    Acta Neurochir Suppl   70   182 - 184   1997

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    DOI: 10.1007/978-3-7091-6837-0_56

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  • Scavenging Effects of Dopamine Agonists on Nitric Oxide Radicals Reviewed

    Sakiko Nishibayashi, Masato Asanuma, Masahiro Kohno, Marvin Gómez-Vargas, Norio Ogawa

    Journal of Neurochemistry   67 ( 5 )   2208 - 2211   1996.11

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    DOI: 10.1046/j.1471-4159.1996.67052208.x

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  • Alterations of cAMP response element-binding activity in the aged rat brain in response to administration of rolipram, a cAMP-specific phosphodiesterase inhibitor Reviewed

    Masato Asanuma, Sakiko Nishibayashi, Emi Iwata, Yoichi Kondo, Tohru Nakanishi, Marvin Gómez Vargas, Norio Ogawa

    Molecular Brain Research   41 ( 1-2 )   210 - 215   1996.9

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    DOI: 10.1016/0169-328x(96)00098-8

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  • Relationship between cholinergic dysfunction and discrimination learning disabilities in Wistar rats following chronic cerebral hypoperfusion Reviewed

    Ken-ichi Tanaka, Norio Ogawa, Masato Asanuma, Yoichi Kondo, Masahiko Nomura

    Brain Research   729 ( 1 )   55 - 65   1996.8

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    The effects of chronic hypoperfusion of cerebral blood flow (CBF) on central cholinergic indices and intellectual functions were investigated in rats. Male Wistar rats, aged 9 weeks, were anesthetized with pentobarbital, and the bilateral common carotid arteries were permanently ligated. Cortical CBF in the hypoperfused rats was markedly decreased at 6 weeks after the operation. In the hypoperfused group, cholinergic indices were changed to consist two phases after the operation, before (acute) and after (chronic) 6 weeks after the operation. At 6 weeks, choline acetyltransferase activity was restored to the sham-operated level compared with the changes in the frontal cortex and thalamus + midbrain at 3 weeks. On the other hand, the maximum number of muscarinic acetylcholine receptors was reduced in the frontal cortex, hippocampus and striatum at 6 weeks and thereafter remained at this low level. In discrimination learning task, the percentage of correct responses in the hypoperfused rats was generally reduced in contrast with that of the sham-operated rats, although the number of total responses were not changed. As a consequence, cholinergic dysfunctions correlate with discrimination learning disabilities in the hypoperfused rats. These findings suggest that the hypoperfused rat may be useful for the cerebrovascular type dementia model to clarify pathophysiology.

    DOI: 10.1016/S0006-8993(96)00400-3

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  • Effects of Bromocriptine on Dopamine Turnover with or without Levodopa Reviewed

    Norio Ogawa, Masato Asanuma, Ken-ichi Tanaka, Koji Matsuura, Kyoko Iida, Mitsutoshi Yamamoto

    Journal of International Medical Research   24 ( 3 )   271 - 277   1996.5

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    Bromocriptine, a dopamine agonist, alleviates symptoms of Parkinson's disease, even when administered alone, and is used for its treatment. Better therapeutic effects are, however, achieved when bromocriptine is used in combination with levodopa. In this study, we examined the biochemical changes caused by bromocriptine administration with and without levodopa, and evaluated the effects of the treatments on dopamine turnover in the mouse striatum. Results show that dopamine turnover is suppressed by the administration of bromocriptine alone with a slight decrease in the amount of dopamine, and dopamine turnover is very strongly promoted by the administration of levodopa. When the two drugs are administered together, bromocriptine enhances the levodopa-induced increase in dopamine turnover in the striatum. These findings indicate that bromocriptine therapy in combination with levodopa enhances the dopaminergic function and suggest that the combination therapy of bromocriptine and levodopa shows good efficacy. The results of this study may, thus, provide a theoretical basis for the combination therapy of bromocriptine and levodopa.

    DOI: 10.1177/030006059602400306

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  • L-DOPA合剤の変更による老齢パーキンソン病患者の問題症状の改善 Invited

    浅沼幹人

    老化と疾患   9 ( 4 )   521 - 525   1996.4

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  • Expression of mRNA encoding neurotrophic factors and its regulation in a hybrid neuronal cell line Reviewed

    Tohru Nakanishi, Kazuhiro Ishii, Nobuyuki Fukushima, Masato Asanuma, Emi Iwata, Norio Ogawa

    Biochemistry and Molecular Biology International   38 ( 4 )   763 - 772   1996.4

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    In a cultured hybrid neuronal cell line (BIM) which was produced between human neuroblastoma cells (IMR32) and thymidine auxotrophs (B3T) of rat nerve-like cells (B103), the mRNAs encoding ciliary neurotrophic factor (CNTF) and neurotrophins were detected by the polymerase chain reaction method. The conditioned medium of BIM cells enhanced choline acetyltransferase (ChAT) activity in septal neurons and survival of-ciliary ganglion neurons. The mRNA expression of CNTF and neurotrophins in BIM cells was differently regulated by the stimulation with cAMP, FGF and retinoic acid. These data suggest multiple regulation and collaboration of neurotrophic factors.

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  • Preventive effects of bifemelane hydrochloride on decreased levels of muscarinic acetylcholine receptor and its mRNA in a rat model of chronic cerebral hypoperfusion Reviewed

    Yoichi Kondo, Norio Ogawa, Masato Asanuma, Koji Matsuura, Sakiko Nishibayashi, Emi Iwata

    Neuroscience Research   24 ( 4 )   409 - 414   1996.3

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    DOI: 10.1016/0168-0102(95)01017-3

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  • Long-term time course of regional changes in cholinergic indices following transient ischemia in the spontaneously hypertensive rat brain Reviewed

    Norio Ogawa, Masato Asanuma, Ken-ichi Tanaka, Hiroshi Hirata, Yoichi Kondo, Masaki Goto, Masamitsu Kawauchi, Toshio Ogura

    Brain Research   712 ( 1 )   60 - 68   1996.3

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    DOI: 10.1016/0006-8993(95)01446-2

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  • Age-related changes in composition of transcription factor, AP-1 complex in the rat brain Reviewed

    Masato Asanuma, Yoichi Kondo, Sakiko Nishibayashi, Emi Iwata, Tohru Nakanishi, Norio Ogawa

    Neuroscience Letters   201 ( 2 )   127 - 130   1995.12

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    DOI: 10.1016/0304-3940(95)12152-8

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  • 脳の老化と生化学 Invited

    浅沼幹人, 小川紀雄

    臨床と研究   72 ( 11 )   2654 - 2658   1995.11

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  • High DNA-binding activity of transcription factor NF-κB in synovial membranes of patients with rheumatoid arthritis. Reviewed

    Hiroshi Asahara, Masato Asanuma, Norio Ogawa, Sakiko Nishibayashi, Hajime Inoue

    Biochemistry and Molecular Biology International   37 ( 5 )   827 - 832   1995.11

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    Our objective was to clarify the DNA-binding activity of transcription factor NF-kappa B as related to cytokine induction in the synovium of patients with rheumatoid arthritis (RA) and osteoarthritis (OA). Synovial membranes were obtained during arthroplasty of the knee from 7 patients with RA and 4 patients with OA. Nuclear extracts obtained from the synovial membranes were examined by electrophoretic mobility shift assay to determine the DNA-binding activity of NF-kappa B. Markedly high DNA-binding activity of NF-kappa B was detected in the synovial membranes of RA patients, while virtually no activity was observed in those of OA patients. These results suggest that the high induction of NF-kappa B in the nuclear extracts may be relatively specific to synovial membranes in RA. NF-kappa B may regulate the production of cytokines at the site of synovial inflammation.

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  • Effects of single cyclosporin A pretreatment on pentylenetetrazol-induced convulsion and on TRE-binding activity in the rat brain Reviewed

    Masato Asanuma, Sakiko Nishibayashi, Yoichi Kondo, Emi Iwata, Masaaki Tsuda, Norio Ogawa

    Molecular Brain Research   33 ( 1 )   29 - 36   1995.10

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    DOI: 10.1016/0169-328x(95)00102-x

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  • M1 Receptors in Blood Pressure–Controlled Ischemic Spontaneously Hypertensive Rats Reviewed

    Hiroshi Hirata, Masato Asanuma, Ken-ichi Tanaka, Yoichi Kondo, Norio Ogawa

    Stroke   26 ( 7 )   1268 - 1272   1995.7

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    <italic>Background and Purpose</italic>
    Hypertension is a primary aggravating factor in cerebral infarction. An acute rise in blood pressure (BP) at the time of a stroke may be harmful to the brain in a hypertensive subject because both cerebral vascular structure and function are altered by hypertension. Muscarinic M
    1
    receptors are concerned with memory and learning. We aimed to evaluate the effect of controlling BP in hypertensive subjects at the time of stroke with a biochemical index of brain damage.




    <italic>Methods</italic>
    We gave a single dose of either the antihypertensive α-blocker phentolamine (2 mg/kg IP) or the calcium antagonist nicardipine (2 mg/kg IP) at the start of bilateral carotid artery occlusion to spontaneously hypertensive rats undergoing 3 hours of transient ischemia; we measured the time course of mean BP (MBP) and changes in the M
    1
    receptor and its mRNA in three brain regions 2 weeks after the transient ischemia.




    <italic>Results</italic>
    Administration of phentolamine or nicardipine not only significantly suppressed the ischemia-induced rise of MBP, it actually decreased MBP during ischemia. In an ischemic control group, M
    1
    receptor binding decreased in the frontal cortex and M
    1
    receptor mRNA increased in the hippocampus 2 weeks after the ischemia. In contrast, both phentolamine- and nicardipine-treated ischemic rats showed no changes in either index compared with sham-operated controls.




    <italic>Conclusions</italic>
    Controlling BP during an ischemic insult attenuates ischemia-induced damage of M
    1
    receptors in the brain of spontaneously hypertensive rats. These results suggest that a rapid intensive increase of BP at the time of a stroke may exacerbate brain damage in hypertensive individuals.

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  • 神経変性過程における免疫制御薬シクロスポリンAの効果 Invited

    小川紀雄, 浅沼幹人

    Dementia   9 ( 2 )   153 - 161   1995.4

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  • Cholecystokinin alterations and effects of levodopa administration in the MPTP-treated mouse brain Reviewed

    Emi Iwata, Masato Asanuma, Yoichi Kondo, Sakiko Nishibayashi, Koji Matsuura, Norio Ogawa

    Research Communications in Molecular Pathology and Pharmacology   88 ( 1 )   31 - 38   1995.4

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    To clarify the effects of levodopa administration on MPTP-induced alterations in neuropeptides, we examined the effects of repeated levodopa injections (200 mg/kg i.p.) for 2 weeks starting 4 weeks after 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) treatment (30 mg/kg i.p. twice/day for 5 days) on cholecystokinin-octapeptide (CCK-8), substance P (SP) and thyrotropin-releasing hormone (TRH) concentrations at 6 weeks after the MPTP treatment. In the striatum, CCK-8 significantly but slightly decreased in the MPTP-treated mice, coinciding with the MPTP-induced marked reduction of dopamine (DA). This considerable reduction of striatal CCK-8 may result from the selectivity of MPTP since the mesolimbic DA neurons coexisting with CCK-8 are intact with the MPTP treatment. Furthermore, this MPTP-induced decrease in CCK-8 persisted with repeated levodopa administration; therefore, the ineffectiveness of the levodopa treatment may have been be due to the degeneration of the nigrostriatal DA neurons. SP and TRH contents showed little or no change with levodopa treatment in the MPTP-treated mouse brain. The CCK-8 level decreased in the thalamus+midbrain, hippocampus and hindbrain of the MPTP + levodopa-treated group, although there were no changes in the MPTP-treated controls. These results suggest that DAergic neurons, except those in the nigrostriatum, strongly interact with the CCK neurons in these brain regions.

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  • Protective effects of pergolide on dopamine levels in the 6-hydroxydopamine-lesioned mouse brain Reviewed

    Masato Asanuma, Norio Ogawa, Sakiko Nishibayashi, Motoko Kawai, Yoichi Kondo, Emi Iwata

    Archives Internationales de Pharmacodynamie et de Therapie   329 ( 2 )   221 - 230   1995.3

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    Pergolide, along with bromocriptine and lisuride, is one of the most active dopamine receptor agonists. To determine whether or not pergolide protects against dopaminergic neuronal damage, via its activity on monoamine metabolism, we studied the effects of pergolide pretreatment on changes in monoamines and their metabolites in the mouse striatum after intracerebroventricular injection of 6-hydroxydopamine with pretreatment of desipramine. After intracerebroventricular administration of 6-hydroxydopamine (40 mu g) in mice, the levels of dopamine and its metabolites (DOPAC, HVA) in the striatum rapidly decreased to 49%, 29% and 68%, respectively, of the naive controls at week 1 but then gradually recovered to control levels at weeks 2 and 4. Repeated pretreatment with pergolide (0.5 mg/kg, i.p.) for 7 days before administration of 6-hydroxydopamine, almost completely protected against reduction in striatal dopamine and its metabolites 1 week after injection of 6-hydroxydopamine. Therefore, pergolide could normalize the decreased dopamine synthesis or storage, and has a neuroprotective effect against dopaminergic dysfunction induced by the neurotoxin, 6-hydroxydopamine. Although we found that pergolide did not show radical scavenging activity in an in vitro system that generated hydroxyl radicals, it has been reported in vivo that pergolide treatment may induce Cu/Zn superoxide dismutase in the rat striatum. Considering these findings, pergolide may well be protective to dopaminergic neurons, largely because of its effects on presynaptic autoreceptors and on its induction of Cu/Zn superoxide dismutase. Further research on the neuroprotective effects of pergolide in Parkinson disease models, by injection of 6-hydroxydopamine, is needed to clarify its mechanism of action on dopaminergic indices.

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  • Cyclosporin A prevents ischemia-induced reduction of muscarinic acetylcholine receptors with suppression of microglial activation in gerbil hippocampus Reviewed

    Yoichi Kondo, Norio Ogawa, Masato Asanuma, Sakiko Nishibayashi, Emi Iwata, Akitane Mori

    Neuroscience Research   22 ( 1 )   123 - 127   1995.3

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    DOI: 10.1016/0168-0102(95)00878-w

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  • Regional Differences in Late-Onset Iron Deposition, Ferritin, Transferrin, Astrocyte Proliferation, and Microglial Activation after Transient Forebrain Ischemia in Rat Brain Reviewed

    Yoichi Kondo, Norio Ogawa, Masato Asanuma, Zensuke Ota, Akitane Mori

    Journal of Cerebral Blood Flow & Metabolism   15 ( 2 )   216 - 226   1995.3

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    With use of iron histochemistry and immuno-histochemistry, regional changes in the appearance of iron, ferritin, transferrin, glial fibrillary acidic protein–positive astrocytes, and activated microglia were examined from 1 to 24 weeks after transient forebrain ischemia (four-vessel occlusion model) in rat brain. Expression of the C3bi receptor and the major histocompatibility complex class II antigen was used to identify microglia. Neuronal death was confirmed by hematoxylin–eosin staining only in pyramidal cells of the hippocampal CA, region, which is known as the area most vulnerable to ischemia. Perls' reaction with 3,3′-diaminobenzidine intensification revealed iron deposits in the CA, region after week 4, which gradually increased and formed clusters by week 24. Iron also deposited in layers III-V of the parietal cortex after week 8 and gradually built up as granular deposits in the cytoplasm of pyramidal cells in frontocortical layer V. An increasing astroglial reaction and the appearance of ferritin-immunopositive microglia paralleled the iron accumulation in the hippocampal CA, region, indicating that iron deposition was probably produced in the process of gliosis. Neither neuronal death nor atrophy was found in the cerebral cortex. Nevertheless, an astroglial and ferritin-immunopositive microglial reaction became evident at week 8 in the parietal cortex. On the other hand, the granular iron deposition in the pyramidal neurons of frontocortical layer V was not accompanied by any glial reaction in the chronic stage of ischemia. Three different types of iron deposition in the chronic phase after transient forebrain ischemia were shown in this study. In view of the neuronal damage caused by iron-catalyzed free radical formation, the late-onset iron deposition may be relevant to the pathogenesis of the chronic brain dysfunction seen at a late stage after cerebral ischemia.

    DOI: 10.1038/jcbfm.1995.27

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  • Angiotensin II Induces in vivo c-fosExpression from Rat Renal Cortex and Medulla Reviewed

    Teruaki Omiya, Takayoshi Yamauchi, Toshio Ogura, Masato Asanuma, Zensuke Ota

    Renal Physiology and Biochemistry   18 ( 2 )   81 - 88   1995.3

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    DOI: 10.1159/000173903

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  • Neuropeptide levels in discrete brain regions in the iminodipropionitrile-induced persistent dyskinesia rat model Reviewed

    Yoshiro Kawada, Norio Ogawa, Masato Asanuma, Akitane Mori

    Regulatory Peptides   55 ( 1 )   103 - 110   1995.1

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    DOI: 10.1016/0167-0115(94)00105-7

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  • Effects of repeated injection of cyclosporin A on pentylenetetrazol-induced convulsion and cyclophilin mRNA levels in rat brain Reviewed

    Masato Asanuma, Norio Ogawa, Sakiko Nishibayashi, Yoichi Kondo, Akitane Mori

    Neurochemical Research   20 ( 1 )   101 - 105   1995.1

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    DOI: 10.1007/bf00995159

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  • 老齢ラット脳内における転写制御因子AP-1のFos-Jun/Jun dimer比の変化 Reviewed

    浅沼幹人, 近藤洋一, 西林佐紀子, 岩田恵美, 松浦弘治, 小川紀雄, 森 昭胤

    Neurosciences   21   125 - 128   1995

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  • Chronic effects of transient forebrain ischemia on monoamines in the spontaneously hypertensive rat brain Reviewed

    Sakiko Nishibayashi, Masato Asanuma, Yoichi Kondo, Emi Iwata, Koji Matsuura, Toshio Ogura, Norio Ogawa

    Biogenic Amines   11 ( 2 )   187 - 194   1995

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    Using the 3-hr common carotid occlusion model in spontaneously hypertensive rats (SHRs), we investigated the changes in monoamines and their metabolites up to the chronic phase, 6 mouths after the transient forebrain ischemia, in various brain regions. In the striatum, the levels of dopamine (DA) at the 3rd week and serotonin (5-HT) at the 2nd week were 1.6-fold and 2.4-fold higher than the levels in the respective sham-operated controls coinciding with increases in their metabolites, homovanillic acid and 5-hydroxyindoleacetic acid. However, these marked increases in both transmitters were transient aid their levels recovered to the sham-operated levels. This transient increase in DA release in the striatum may be caused by ischemia-induced disruption of nerve endings, and may aggravate tissue damage in the striatum at the chronic phase after ischemia. Transient or lasting changes in noradrenaline, DA, 5-HT and their metabolites were also observed in other brain regions, the thalamus+midbrain and the hippocampus of SHRs after transient ischemia. These ischemia-induced alterations in monoamines at the chronic phase may be partly involved in the late-onset sequelae seen in the cerebrovascular disorders.

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  • 中枢神経における転写制御因子結合活性に対する酸化的ストレスの影響 Reviewed

    岩田恵美, 浅沼幹人, 西林佐紀子, 近藤洋一, 松浦弘治, 小川紀雄, 森 昭胤

    Neurosciences   21   77 - 80   1995

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  • ラット脳血流慢性低潅流時におけるアセチルコリン系の変化 Reviewed

    西林佐紀子, 浅沼幹人, 近藤洋一, 岩田恵美, 松浦弘治, 飯田享子, 小川紀雄, 森 昭胤

    Neurosciences   21   109 - 112   1995

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  • Regional changes in α-tubulin and β-actin mRNA accumlations after transient ischemia in spontaneously hypertensive rat brains Reviewed

    Yoichi Kondo, Norio Ogawa, Masato Asanuma, Hiroshi Hirata, Sakiko Nishibayashi, Akitane Mori

    Research Communications in Molecular Pathology and Pharmacology   86 ( 2 )   139 - 153   1994.11

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    Regional changes in the mRNA accumulations for cytoskeletal proteins alpha-tubulin and beta-actin were examined by in situ hybridization and Northern blot analysis in spontaneously hypertensive rat brains at chronic stages after 3 hours of transient ischemia. alpha-Tubulin mRNA accumulations showed no significant change at 2 weeks after transient ischemia except for a significant decrease in the frontal cortex (9.7%, p &lt; 0.01) coinciding with ischemia induced histological changes. beta-Actin mRNA level was significantly increased in the parietal cortex (8.5%), septum (10.0%), amygdala (11.0%), CA4 area (5.8%) and the dentate gyrus (7.5%) of the hippocampus at 2 weeks after recirculation compared with a sham-operated control group (p&lt;0.01). The ischemic areas of hippocampal and frontocortical lesions receive afferent neurons from those regions where beta-actin mRNA was increased, suggesting that ischemia-induced increases in beta-actin mRNA may reflect actin synthesis in these neurons to compensate for lost synaptic connections. Two cytoskeletal mRNA concentrations reacted differently to cerebral ischemia, and did not parallel histological signs of ischemia either temporally or spatially.

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  • Chronic administration of acetylcholinesterase inhibitor in the senescent Rat brain Reviewed

    Ken-ichi Tanaka, Norio Ogawa, Masato Asanuma, Yoichi Kondo, Akitane Mori

    Neurobiology of Aging   15 ( 6 )   721 - 725   1994.11

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    DOI: 10.1016/0197-4580(94)90054-x

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  • Tubulin and actin mRNAs in the young-adult and the aged rat brain: effects of repeated administration with bifemelane hydrochloride Reviewed

    Sakiko Nishibayashi, Norio Ogawa, Masato Asanuma, Yoichi Kondo, Akitane Mori

    Archives of Gerontology and Geriatrics   19 ( 3 )   265 - 272   1994.11

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    DOI: 10.1016/0167-4943(94)00572-9

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  • Bromocriptine protects mice against 6-hydroxydopamine and scavenges hydroxyl free radicals in vitro Reviewed

    Norio Ogawa, Ken-ichi Tanaka, Masato Asanuma, Motoko Kawai, Toshiki Masumizu, Masahiro Kohno, Akitane Mori

    Brain Research   657 ( 1-2 )   207 - 213   1994.9

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    DOI: 10.1016/0006-8993(94)90969-5

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  • Reduced choline acetyltransferase activity and muscarinic M1 receptor levels in aged Fisher 344 rat brains did not parallel their respective mRNA levels Reviewed

    Norio Ogawa, Masato Asanuma, Yoichi Kondo, Sakiko Nishibayashi, Akitane Mori

    Brain Research   658 ( 1-2 )   87 - 92   1994.9

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    DOI: 10.1016/s0006-8993(09)90013-0

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  • Effects of Repeated Immunosuppressant Treatment on Rat Pentylenetetrazol-Induced Convulsion Reviewed

    Masato Asanuma, Yoichi Kondo, Norio Ogawa, Akitane Mori

    Japanese Journal of Psychiatry and Neurology   48 ( 2 )   281 - 284   1994.6

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    DOI: 10.1111/j.1440-1819.1994.tb03068.x

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  • Amantadine(Symmetrel)の使い方と問題点 Invited

    浅沼幹人, 小川紀雄

    内科   73 ( 5 )   868 - 870   1994.5

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  • Changes in lipid peroxidation, Cu/Zn-superoxide dismutase and its mRNA following an intracerebroventricular injection of 6-hydroxydopamine in mice Reviewed

    Norio Ogawa, Masato Asanuma, Yoichi Kondo, Hiroshi Hirata, Sakiko Nishibayashi, Akitane Mori

    Brain Research   646 ( 2 )   337 - 340   1994.5

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    DOI: 10.1016/0006-8993(94)90102-3

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  • Iminodipropionitrile投与によって発症させたジスキネジアモデルラットの脳内神経ペプチドの変化 Reviewed

    河田義郎, 小川紀雄, 浅沼幹人, 森 昭胤

    Neurosciences   20   41 - 44   1994.4

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  • Differential effects of chronic l-DOPA treatment on lipid peroxidation in the mouse brain with or without pretreatment with 6-hydroxydopamine Reviewed

    Norio Ogawa, Masato Asanuma, Yoichi Kondo, Yoshiro Kawada, Mitsutoshi Yamamoto, Akitane Mori

    Neuroscience Letters   171 ( 1-2 )   55 - 58   1994.4

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    DOI: 10.1016/0304-3940(94)90603-3

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  • 虚血と神経毒による晩発性脳障害 Invited

    小川紀雄, 浅沼幹人, 水川公直

    老年期痴呆研究会誌   6   16 - 19   1994.2

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  • Acetylcholinesterase inhibitor ENA-713 protects against ischemia-induced decrease in pre- and postsynaptic cholinergic indices in the gerbil brain following transient ischemia Reviewed

    Ken-ichi Tanaka, Norio Ogawa, Kiminao Mizukawa, Masato Asanuma, Yoichi Kondo, Sakiko Nishibayashi, Akitane Mori

    Neurochemical Research   19 ( 2 )   117 - 122   1994.2

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    DOI: 10.1007/bf00966804

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  • Pitfalls in Assessment of c-fos mRNA Expression in the Brain: Effects of Animal Handling Reviewed

    Masato Asanuma, Norio Ogawa

    Reviews in the Neurosciences   5 ( 2 )   1994.1

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    DOI: 10.1515/revneuro.1994.5.2.171

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  • Effect of vagatomy on hyperactivity and increased dopamine turnover induced by intraperitoneal administration of thyrotropin-releasing hormone Reviewed

    Norio Ogawa, Masato Asanuma, Yoichi Kondo, Hiroshi Hirata, Naoharu Nakayama, Akitane Mori

    Brain Research   633 ( 1-2 )   167 - 170   1994.1

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    DOI: 10.1016/0006-8993(94)91536-9

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  • 脳障害過程での免疫系の関与-免疫抑制薬cyclosporine Aを用いた実験的研究- Reviewed

    小川紀雄, 浅沼幹人, 近藤洋一

    日本神経精神薬理学会雑誌   14   377 - 381   1994

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  • Alterations in the binding of the phosphodiesterase inhibitor, rolipram, after transient ischemia in the gerbil brain Reviewed

    Masato Asanuma, Norio Ogawa, Hiroshi Hirata, Yoichi Kondo, Sakiko Nishibayashi, Mitsutoshi Yamamoto, Akitane Mori

    Research Communications in Molecular Pathology and Pharmacology   82 ( 3 )   279 - 285   1993.12

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    To determine ischemia-induced changes in phosphodiesterase (PDE), changes in the membranous binding sites of rolipram, a cAMP-selective PDE inhibitor, were examined in the gerbil brain following transient 5 min forebrain ischemia. Coinciding with the delayed neuronal death (DND) in the hippocampal CA1 region, affinities for cerebral rolipram bindings decreased on Day 4, when intrinsic cAMP, substrate for PDE, might increase. The number of rolipram binding sites was significantly reduced in the hippocampus on Day 14, despite the lack of change on Day 4. This reduction in rolipram binding was in agreement with the previously reported late onset reduction of muscarinic receptors, progressing more slowly than DND. Slowly progressive mechanisms may be involved in the ischemia-induced reduction of the hippocampal rolipram binding sites which may be PDEs

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  • ドキサゾシン投与において脳血流増加を認めた脳梗塞合併高血圧症の一例 Reviewed

    山本光利, 浅沼幹人, 小川紀雄

    臨床と研究   70 ( 9 )   2975 - 2978   1993.9

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  • Abnormalities in muscarinic cholinergic receptors and their G-protein coupling systems in the cerebral frontal cortex in Alzheimer's disease Reviewed

    Norio Ogawa, Kiminao Mizukawa, Masato Asanuma, Ichiro Kanazawa

    Archives of Gerontology and Geriatrics   17 ( 2 )   77 - 89   1993.9

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    DOI: 10.1016/0167-4943(93)90040-o

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  • Rapid response of striatal muscarinic M1-receptor mRNA to muscarinic cholinergic agents in rat brain Reviewed

    Hsi-hsien Chou, Norio Ogawa, Masato Asanuma, Hiroshi Hirata, Yoichi Kondo, Akitane Mori

    Molecular Brain Research   19 ( 3 )   211 - 214   1993.8

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    DOI: 10.1016/0169-328x(93)90028-n

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  • 脊髄小脳変性症/生化学的な進歩 Invited

    浅沼幹人, 小川紀雄

    Clinical Neuroscience   11 ( 6 )   626 - 629   1993.6

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  • Regional changes in neuropeptide levels after 5,7-dihydroxytryptamine-induced serotonin depletion in the rat brain Reviewed

    Yoichi Kondo, Norio Ogawa, Masato Asanuma, Hiroshi Hirata, Ken-ichi Tanaka, Yoshiro Kawada, Akitane Mori

    Journal of Neural Transmission   92 ( 2-3 )   151 - 157   1993.6

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    DOI: 10.1007/bf01244874

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  • Effects of the acetylcholinesterase inhibitor ENA-713 on ischemia-induced changes in acetylcholine and aromatic amine levels in the gerbil brain Reviewed

    Ken-ichi Tanaka, Norio Ogawa, Masato Asanuma, Hiroshi Hirata, Yoichi Kondo, Naoharu Nakayama, Akitane Mori

    Archives Internationales de Pharmacodynamie et de Therapie   323 ( 1-2 )   85 - 96   1993.5

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    The effects of a new acetylcholinesterase inhibitor, ENA-713, on ischemia-induced changes in acetylcholine, monoamines, and their metabolites, were studied in the gerbil. ENA-713 (0.2 mg/kg) or saline was administered intraperitoneally to gerbils 30 min before induction of cerebral ischemia by bilateral carotid occlusion. Pretreatment with ENA-713 mitigated the ischemia-induced abnormalities of the cholinergic, dopaminergic and serotoninergic systems in the gerbil brain, although it had virtually no effect on acetylcholine, monoamines, or their metabolites in any region of the normal gerbil brain. These findings suggest that ENA-713 has beneficial effects against ischemia-induced cerebral disorders. Thus, ENA-713 seems to be promising as a preventive or therapeutic agent for cerebrovascular dementia due to cerebral ischemia and might be useful for the treatment of Alzheimer-type dementia which is associated with multiple neurotransmitter abnormalities in the brain.

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  • 一過性脳虚血後の晩発性ムスカリン性受容体減少に対する免疫抑制剤Cyclosporin Aの阻止効果 Reviewed

    小川紀雄, 浅沼幹人, 近藤洋一, 水川公直, 森 昭胤

    Neurosciences   19 ( 1 )   81 - 84   1993.4

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  • The preventive effect of cyclosporin A, an immunosuppressant, on the late onset reduction of muscarinic acetylcholine receptors in gerbil hippocampus after transient forebrain ischemia Reviewed

    Norio Ogawa, Ken-ichi Tanaka, Yoichi Kondo, Masato Asanuma, Kiminao Mizukawa, Akitane Mori

    Neuroscience Letters   152 ( 1-2 )   173 - 176   1993.4

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    DOI: 10.1016/0304-3940(93)90511-i

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  • ニユーロトランスミッターのレセプター結合実験法 Invited

    浅沼幹人, 小川紀雄

    実験医学   11 ( 3 )   216 - 223   1993.3

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  • 脳に対するカルシウム拮抗薬の功罪-カルシウム拮抗薬のドーパミン受容体に対する作用- Invited

    浅沼幹人

    Clinical Calcium   3 ( 3 )   97 - 102   1993.3

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  • Amytriptyline投与により無動・姿勢保持障害・歩行障害等の症状改善と同時に前頭葉脳血流低下の著明な改善を認めた進行性核上麻痺の一例 Reviewed

    浅沼幹人, 平田 洋, 近藤洋一, 小川紀雄

    臨床神経学   33 ( 3 )   317 - 321   1993.3

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  • Effects of repeated administration of rolipram, a cAMP-specific phosphodiesterase inhibitor, on acetylcholinergic indices in the aged rat brain Reviewed

    Masato Asanuma, Norio Ogawa, Yoichi Kondo, Hiroshi Hirata, Akitane Mori

    Archives of Gerontology and Geriatrics   16 ( 2 )   191 - 198   1993.3

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    DOI: 10.1016/0167-4943(93)90009-7

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  • Cholinergic deficits in aged rat brain are corrected with nicergoline Reviewed

    Norio Ogawa, Masato Asanuma, Hiroshi Hirata, Yoichi Kondo, Yoshiro Kawada, Akitane Mori

    Archives of Gerontology and Geriatrics   16 ( 2 )   103 - 110   1993.3

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    DOI: 10.1016/0167-4943(93)90001-x

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  • 大腸ファイバー検査直後よりwearing off現象の著明な改善のみられたParkinson病 Reviewed

    近藤洋一, 平田 洋, 浅沼幹人, 小川紀雄, 太田善介

    神経内科   38 ( 3 )   291 - 292   1993.3

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  • 脳血管障害後遺症に対する塩酸ビフェメラン長期投与の効果 Reviewed

    浅沼幹人, 平田 洋, 近藤洋一, 小川紀雄

    臨床と研究   70 ( 2 )   572 - 576   1993.2

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  • Effect of chronic ceruletide treatment on dopaminergic neurotransmitters, receptors and their mRNAs in the striatum of rats with dyskinesia induced by iminodipropionitrile Reviewed

    Hiroshi Hirata, Norio Ogawa, Masato Asanuma, Zensuke Ota, Akitane Mori

    Brain Research   604 ( 1-2 )   197 - 204   1993.2

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    DOI: 10.1016/0006-8993(93)90369-x

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  • Ischemia-induced changes in α-tubulin and β-actin mRNA in the gerbil brain and effects of bifemelane hydrochloride Reviewed

    Masato Asanuma, Norio Ogawa, Hiroshi Hirata, Hsi-hsien Chou, Yoichi Kondo, Akitane Mori

    Brain Research   600 ( 2 )   243 - 248   1993.1

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    DOI: 10.1016/0006-8993(93)91379-7

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  • 脳血管障害総論/脳神経化学の進歩 Invited

    小川紀雄, 浅沼幹人, 近藤洋一

    日本臨床   51(1993年増刊上巻)   61 - 68   1993

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  • Effective Treatment by Bifemerane Hydrochloride for Emotional Incontinence and Regional Blood Flow in Patient with Cerebral Infarction Reviewed

    M. Yamamoto, M. Asanuma, N. Ogawa

    Nippon Ronen Igakkai Zasshi. Japanese Journal of Geriatrics   30 ( 1 )   70 - 73   1993

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    The authors report that bifemerane hydrochloride treatment improved emotional incontinence in patient with cerebral infarction. Before and after bifemerane hydrochloride treatment, 99mTc-HM PAO single photon emission CT (SPECT) was performed. After treatment, regional cerebral blood flows (CBF) in frontal lobe area increased selectively. These findings suggest that emotional incontinence and decreased CBF of the frontal lobe area were closely associated in this case. © 1993, The Japan Geriatrics Society. All rights reserved.

    DOI: 10.3143/geriatrics.30.70

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  • Degeneration of dopaminergic neurons and free radicals: Possible participation of levodopa Reviewed

    Norio Ogawa, Rei Edamatsu, Kiminao Mizukawa, Masato Asanuma, Masahiro Kohno, Akitane Mori

    Advances in Neurology   60   242 - 250   1993

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  • Comparison of the effects of bifemelane hydrochloride, idebenone and indeloxazine hydrochloride on ischemia-induced changes in brain monoamines and their metabolites in gerbils Reviewed

    Kumiko Haba, Norio Ogawa, Masato Asanuma, Hiroshi Hirata, Akitane Mori

    Journal of Neural Transmission   88 ( 3 )   187 - 198   1992.10

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    DOI: 10.1007/bf01244732

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  • Opposite effects of rough and gentle handling with repeated saline administration on c-fos mRNA expression in the rat brain Reviewed

    Masato Asanuma, Norio Ogawa, Hiroshi Hirata, Hsi-hsien Chou, Ken-ichi Tanaka, Akitane Mori

    Journal of Neural Transmission   90 ( 3 )   163 - 169   1992.10

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    DOI: 10.1007/bf01250958

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  • Muscarinic cholinergic receptor-mediated modulation on striatal c-fos mRNA expression induced by levodopa in rat brain Reviewed

    Hsi-hsien Chou, Norio Ogawa, Masato Asanuma, Hirata Hirata, Akitane Mori

    Journal of Neural Transmission   90 ( 3 )   171 - 181   1992.10

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    DOI: 10.1007/bf01250959

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  • Post-ischemic administration of bifemelane hydrochloride prohibits ischemia-induced depletion of the muscarinic M1-receptor and its mRNA in the gerbil hippocampus Reviewed

    Norio Ogawa, Masato Asanuma, Kiminao Mizukawa, Hirata Hirata, Hsi-hsien Chou, Akitane Mori

    Brain Research   591 ( 1 )   171 - 175   1992.9

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    DOI: 10.1016/0006-8993(92)90993-j

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  • 長期パーキンソン病患者に対するタンパク質摂取制限療法の効果,副作用および適応に関する検討 Reviewed

    平田 洋, 浅沼幹人, 近藤洋一, 小川紀雄

    臨床神経学   32 ( 9 )   973 - 978   1992.9

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  • Effects of chronic codergocrine mesylate administration on the brain somatostatinergic system in aged rats Reviewed

    Ken-ichi Tanaka, Norio Ogawa, Masato Asanuma, Hiroshi Hirata, Yoichi Kondo, Hsi-hsien Chou, Akitane Mori

    Archives of Gerontology and Geriatrics   15 ( 2 )   133 - 139   1992.9

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    DOI: 10.1016/0167-4943(92)90013-t

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  • 薬物療法-L-DOPAを中心に Invited

    浅沼幹人, 小川紀雄

    MEDICO   23 ( 7 )   9997 - 10001   1992.7

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  • Effects of chronic catecholamine depletions on muscarinic M1-receptor and its mRNA in rat brain Reviewed

    Masato Asanuma, Norio Ogawa, Kumiko Haba, Hiroshi Hirata, Akitane Mori

    Journal of the Neurological Sciences   110 ( 1-2 )   205 - 214   1992.7

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    DOI: 10.1016/0022-510x(92)90029-k

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  • Effects of chronic bifemelane hydrochloride administration on receptors for N-methyl-d-aspartate in the aged-rat brain Reviewed

    Norio Ogawa, Kiminao Mizukawa, Kumiko Haba, Masato Asanuma, Akitane Mori

    Neurochemical Research   17 ( 7 )   687 - 691   1992.7

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    DOI: 10.1007/bf00968006

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  • Effects of dihydroergotoxine on central cholinergic neuronal systems and discrimination learning test in aged rats Reviewed

    Norio Ogawa, Masahiko Nomura, Kumiko Haba, Masato Asanuma, Ken-ichi Tanaka, Koji Hori, Akitane Mori

    Brain Research   586 ( 2 )   229 - 234   1992.7

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    DOI: 10.1016/0006-8993(92)91631-n

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  • 脳梗塞後遺症における脳循環改善薬の有効症状スペクトラムの比較

    小川紀雄, 浅沼幹人, 平田 洋, 近藤洋一

    Prog. Med.   12 ( 6 )   1337 - 1344   1992.6

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  • Age-Related Changes in Cerebrospinal Fluid γ-Aminobutyric Acid Concentration Reviewed

    Haruhiko Takayama, Norio Ogawa, Mitsutoshi Yamamoto, Masato Asanuma, Hiroshi Hirata, Zensuke Ota

    Clinical Chemistry and Laboratory Medicine   30 ( 5 )   1992.5

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    DOI: 10.1515/cclm.1992.30.5.271

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  • Late onset and long-lasting suppressive effects of ceruletide, an analogue of cholecystokinin, on c-fos mRNA expression in the rat striatum Reviewed

    Masato Asanuma, Norio Ogawa, Hiroshi Hirata, Kumiko Haba, Hsi-hsien Chou, Akitane Mori

    Neuroscience Letters   138 ( 2 )   233 - 236   1992.4

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    DOI: 10.1016/0304-3940(92)90922-t

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  • Effects of propentophylline on ischemia induced loss of muscarinic cholinergic receptor binding in the gerbil hippocampus Reviewed

    Hiroshi Hirata, Norio Ogawa, Kumiko Haba, Masato Asanuma, Hsi-hsien Chou, Akitane Mori

    Research Communications in Chemical Pathology and Pharmacology   75 ( 3 )   365 - 368   1992.3

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    Super-delayed loss of muscarinic-1 (M1) receptors and the protective effect of propentofylline on these changes were examined in the gerbil hippocampus after transient ischemia with radioactive pirenzepine. M1 receptors were markedly decreased in the gerbil hippocampus 14 days after transient ischemia. Single administration of propentofylline (20mg/kg, ip) just after transient ischemia almost completely prevented the ischemia-induced decrease in the number of M1 receptors, and had no effect in sham-operated controls. These findings suggest that one of the therapeutic efficacies of propentofylline is the result of the normalization of the dysfunction of the acetylcholine neuronal system in cerebrovascular disease.

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  • Changes of neuropeptides and their receptors in experimental stroke gerbil brains Reviewed

    Kumiko Haba, Norio Ogawa, Masato Asanuma, Hiroshi Hirata, Yukiko H. Sora, Akitane Mori

    Journal of the Neurological Sciences   108 ( 1 )   88 - 92   1992.3

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    DOI: 10.1016/0022-510x(92)90192-n

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  • 多発性脳梗塞におけるnicergolineの臨床効果と123I-IMP SPECT上の脳血流改善

    小川紀雄, 浅沼幹人, 平田 洋, 太田善介

    臨床と研究   69 ( 3 )   949 - 957   1992.3

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  • Development of a Simple Spasticity Quantification Method: Effects of Tizanidine on Spasticity in Patients with Sequelae of Cerebrovascular Disease Reviewed

    Norio Ogawa, Masato Asanuma, Hiroshi Hiraata, Zensuke Ota, Yasuhide Yamawaki, Mitsutoshi Yamamoto

    Journal of International Medical Research   20 ( 1 )   78 - 86   1992.2

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    A simple method that can be performed at the bedside using a spring balance was developed in order to quantify spasticity. The effects of tizanidine on spasticity were evaluated in 30 patients with sequelae of cerebrovascular disease using this method. Treatment with tizanidine was effective in 60% of the patients; there were high correlations between spasticity before and after tizanidine administration and the severity of symptoms and also between the degree of improvement in spasticity and in that of the symptoms. Atonic seizures, due to overdose of tizanidine, were observed in only one patient. The simple spasticity quantification method developed was useful for monitoring tizanidine administration in order to prevent drug overdose. The method appears to be very useful for evaluating the degree of spasticity at the bedside and in measuring the effects of antispastic drugs.

    DOI: 10.1177/030006059202000109

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  • Effects of chronic administration of lisuride hydrogen maleate on aromatic amine and metabolite levels in the gerbil brain following bilateral common carotid ligation Reviewed

    Hiroshi Hirata, Norio Ogawa, Kumiko Haba, Masato Asanuma, Hsi-hsien Chou, Akitane Mori

    Archives Internationales de Pharmacodynamie et de Therapie   315 ( 1-2 )   5 - 15   1992.1

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    Cerebral monoaminergic neurotransmitters and their metabolites show various concentration changes in gerbils following bilateral carotid ligation. The present study evaluated the effect of chronic administrations of lisuride hydrogen maleate (lisuride) on these changes. Lisuride (0.01 mg/kg or 0.05 mg/kg) or vehicle was intraperitoneally administered to gerbils for 14 consecutive days before the induction of a 30 min ischemia by bilateral carotid ligation. Animals were sacrified immediately and the levels of dopamine, DOPAC, homovanillic acid, noradrenaline, serotonin and 5-hydroxyindoleacetic acid determined by HPLC in the striatum, cortex, hippocampus and diencephalon/midbrain. Lisuride itself had no effect on any compound determined in any region. In the carotid-ligated gerbil brain, however, lisuride corrected the reduction of dopamine in the striatum, normalized or reduced increases in the (DOPAC + homovanillic acid)/dopamine ratio in the striatum, hippocampus and diencephalon/midbrain, and increased the levels of serotonin in all four regions. The present study, together with previous reports, indicate that lisuride may interfere with ischemia-induced cerebrovascular disturbances and, in such a way, improve some pathological sequelae of cerebrovascular disease.

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  • Effects of bifemelane hydrochloride on loss of N-methyl-D-aspartate receptor and muscarinic cholinergic receptor binding in the gerbil hippocampus after transient ischemia Reviewed

    Masato Asanuma, Norio Ogawa, Kumiko Haba, Hiroshi Hirata, Hsi-hsien Chou, Akitane Mori

    Archives Internationales de Pharmacodynamie et de Therapie   315 ( 1-2 )   16 - 21   1992.1

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    The effects of bifemelane hydrochloride on changes of N-methyl-D-aspartate receptors and muscarinic cholinergic receptors were examined in the gerbil hippocampus after transient ischemia with radioactive-specific ligands. There were marked reductions in both these receptors in the gerbil hippocampus 14 days after transient ischemia, without changes in the respective affinities. Post-ischemia bifemelane treatment almost completely prevented the ischemia-induced decreases in the numbers of these receptors, and had no effect in sham-operated controls. The results of the present study suggest that this drug prevents postsynaptic dysfunction induced by transient ischemia, and may be useful in the therapy of both the chronic and the acute stage of cerebrovascular disease.

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  • 超高齢者の脳血管障害後遺症に対する脳代謝改善薬の有効症状のプロフィールの相違

    浅沼幹人, 平田 洋, 高山晴彦, 更井哲夫, 小川紀雄

    臨床と研究   69 ( 1 )   265 - 275   1992.1

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  • Chronic administration of lisuride hydrogen maleate increases muscarinic acetylcholine receptor binding in aged rat brain Reviewed

    Haruhiko Takayama, Masato Asanuma, Kiminao Mizukawa, Hiroshi Hirata, Hirohiko Sato, Zensuke Ota, Norio Ogawa

    Japanese Journal of Geriatrics   29 ( 1 )   24 - 28   1992.1

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    Changes in the distribution and densities of muscarinic acetylcholine receptors (mACh-R) in young adult and aged rat brain, and the effects of chronic administration of lisuride hydrogen maleate (lisuride) on these changes were studied by in vitro quantitative autoradiography of [3H] quinuclidinyl benzilate binding. mACh-R was relatively higher in the striatum, hippocampus and cerebral cortex in the young adult rats. In contrast, mACh-R binding was markedly reduced in the striatum, accumbens nucleus, amygdaloid nucleus and frontal cerebral cortex of aged rats compared to young adult rats. However, chronic administration of lisuride significantly increased mACh-R binding in the parietal cerebral cortex of aged rats compared to young adult rats. However, chronic administration of lisuride significantly increased mACh-R binding in the parietal cerebral cortex as well as in the above-mentioned regions in aged rats. This lisuride-induced increase in mACh-R of aged rat brain is considered to have important implications concerning the mechanism of therapeutic efficacy of lisuride.

    DOI: 10.3143/geriatrics.29.24

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  • Distinction between declarative memory and procedural memory using 8-arm radial maze task : Biphasic effects of thyrotropin reloading hormone on scopolamine-induced amnesia. Reviewed

    Norio Ogawa, Masato Asanuma, Hiroshi Hirata, Hsi-hsien Chou, Yoichi Kondo, Setsuko Ogawa, Akitane Mori

    Research Communications in Psysiology, Psychiatry and Behavior   17 ( 1-2 )   1 - 15   1992

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  • Distribution of the beta-2 adrenergic receptor messenger RNA in the rat brain by in situ hybridization histochemistry: Effects of chronic reserpine treatment Reviewed

    Masato Asanuma, Norio Ogawa, Kiminao Mizukawa, Kumiko Haba, Hiroshi Hirata, Akitane Mori

    Neurochemical Research   16 ( 12 )   1253 - 1256   1991.12

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    DOI: 10.1007/bf00966654

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  • Calcium antagonist flunarizine hydrochloride affects striatal D2 dopamine receptors in the young adult and aged rat brain Reviewed

    Masato Asanuma, Norio Ogawa, Kumiko Haba, Hiroshi Hirata, Akitane Mori

    Archives of Gerontology and Geriatrics   13 ( 3 )   271 - 278   1991.11

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    DOI: 10.1016/0167-4943(91)90049-v

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  • ソマトスタチン減少剤 Invited

    浅沼幹人, 小川紀雄

    生体の科学   42 ( 5 )   505 - 506   1991.10

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    DOI: 10.11477/mf.2425900277

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  • Effects of beta-adrenergic blocking agents on specific binding of [3H]D-Ala2-Met5-enkephalinamide and [3H]naloxone. Reviewed

    Haruhiko Takayama, Norio Ogawa, Masato Asanuma, Hiroshi Hirata, Toshio Ogura, Zensuke Ota

    Acta Medica Okayama   45 ( 5 )   295 - 299   1991.10

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    DOI: 10.18926/AMO/32199

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  • Dopamine deficiency in the Weaver mutant mouse: An animal model of olivopontocerebeller atrophy Reviewed

    Hsi-hsien Chou, Norio Ogawa, Masato Asanuma, Hiroshi Hirata, Akitane Mori

    Research Communications in Chemical Pathology and Pharmacology   74 ( 1 )   117 - 120   1991.10

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    The dopamine system in weaver mutant mice, a model of cerebellar atrophy, was studied. Dopamine levels of 6-week-old weaver mice were 37%, 44%, 34%, and 41% of levels in age-matched controls in the cerebral cortex, hippocampus, septal region and striatum, respectively. Noradrenaline levels did not differ from controls. This study shows that weaver mice have specific deficiencies in the dopamine system.

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  • Long-lasting effect of ceruletide on dyskinesia and monoaminergic neuronal pathways in rats treated with iminodipropionitrile Reviewed

    Norio Ogawa, Kumiko Haba, Masato Asanuma, Akitane Mori

    Brain Research   556 ( 2 )   271 - 279   1991.8

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    DOI: 10.1016/0006-8993(91)90315-m

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  • 神経伝達物質とパーキンソン病 Invited

    浅沼幹人, 小川紀雄

    臨床成人病   21 ( 7 )   1191 - 1199   1991.7

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  • Chronic Lisuride Hydrogen Maleate Administration Enhances Muscarinic Receptor Binding in Senescent Rat Brain Reviewed

    Hiroshi Hirata, Norio Ogawa, Kiminao Mizukawa, Kumiko Haba, Masato Asanuma, Akitane Mori, Zensuke Ota

    Journal of International Medical Research   19 ( 4 )   318 - 325   1991.7

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    Changes in the regional density of muscarinic-1 (M1) receptors and the effect of lisuride hydrogen maleate on these changes were studied in senescent rat brain by in vitro autoradiography. In young adult controls, M1 receptor binding was most dense in the striatum and hippocampus, followed by the cerebral cortex and amygdala. Binding to M1 receptors was markedly lower in these areas of the senescent brain compared with the young adult brain. These decreases were reversed by intraperitoneal administration of 50 μg/kg·day lisuride for 14 days. The present results indicate that the therapeutic efficacy of lisuride depends on normalization of not only monoamine systems but also acetylcholine systems.

    DOI: 10.1177/030006059101900404

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  • 脳血管障害後遺症における意欲低下・問題行動に対する塩酸インデロキサジンの改善効果

    浅沼幹人, 平田 洋, 高山晴彦, 更井哲夫, 小川紀雄

    Prog. Med.   11 ( 6 )   1527 - 1530   1991.6

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  • イブジラストの脳梗塞症例における脳血流改善作用-SPECTを用いて-

    高山晴彦, 浅沼幹人, 佐藤博彦, 平田 洋, 太田善介, 小川紀雄

    臨床と研究   68 ( 6 )   1857 - 1862   1991.6

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  • Loss of N-methyl-d-aspartate (NMDA) receptor binding in rat hippocampal areas at the chronic stage after transient forebrain ischemia: Histological and NMDA receptor binding studies Reviewed

    Norio Ogawa, Kumiko Haba, Kiminao Mizukawa, Masato Asanuma, Hiroshi Hirata, Akitane Mori

    Neurochemical Research   16 ( 5 )   519 - 524   1991.5

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    DOI: 10.1007/bf00974869

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  • Chronic bifemelane hydrochloride administration enhances muscarinic cholinergic recepotr binding in the senescent rat brain Reviewed

    Norio Ogawa, Kiminao Mizukawa, Kumiko Haba, Masato Asanuma, Akitane Mori

    Journal of Medicine   22 ( 1 )   17 - 27   1991.1

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    In senescent rats, the binding ability of muscarinic cholinergic receptors (MCR) was markedly decreased in the cerebral cortex, hippocampus, thalamus, and the striatum compared with young adult rats. This decrease was markedly improved by chronic administration of bifemelane hydrochloride (bifemelane). In view of the findings that bifemelane markedly inhibits the decrease in acetylcholine (ACh) associated with cerebral ischemia, and that it improves amnesia induced by scopalamine, it may be inferred that bifemelane between in situ malignant melanoma and other melanin-containing in situ malignancies has been presented. All types of malignant melanoma which originate within the epidermis or epithelium have an in situ phase and show horizontal growth, and small early forms defy classification. The classification of the most common types of malignant melanoma has been revised. Although the level of invasion and tumor thickness are useful prognostic and therapeutic parameters, their determination is crude and subject to several shortcomings.

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  • レセルピン慢性投与のアセチルコリン系神経機構に及ぼす影響 Reviewed

    浅沼幹人, 羽場久美子, 小川紀雄, 森 昭胤

    Neurosciences   17 ( 1 )   87 - 90   1991.1

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  • パーキンソン病 Invited

    浅沼幹人, 小川紀雄

    Brain Medical   3 ( 4 )   351 - 358   1991

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  • Super-Delayed Changes of Muscarinic Acetylcholine Receptor in the Gerbil Hippocampus Following Transient Ischemia Reviewed

    Norio Ogawa, Kumiko Haba, Masato Asanuma, Kiminao Mizukawa, Akitane Mori

    Advances in Experimental Medicine and Biology   287   343 - 347   1991

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    DOI: 10.1007/978-1-4684-5907-4_28

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  • Chronic administration of bifemelane hydrochoride increases somatostatin receptor binding in aged rat brain

    H. Sato, K. Mizukawa, N. Ogawa, M. Asanuma, H. Takayama, Z. Ota

    Japanese Journal of Geriatrics   28 ( 1 )   18 - 23   1991

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    DOI: 10.3143/geriatrics.28.18

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  • 神経ペプチドとレセプター

    小川紀雄, 浅沼幹人, 羽場久美子

    内分泌学の進歩   8   55 - 74   1991

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  • Regional responses of rat brain opioid receptors upon castration and testosterone replacement Reviewed

    Haruhiko Takayama, Norio Ogawa, Masato Asanuma, Zensuke Ota

    Research Communications in Chemical Pathology and Pharmacology   70 ( 3 )   355 - 358   1990.12

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    Regional responses of rat brain opioid receptors (Op-Rs) upon castration and testosterone replacement were studied using [H-3]naloxone (NAL) binding for u-type and [H-3]D-Ala2-methionine-enkephalin (ENK) binding for delta-type Op-R. Castration itself produced an increase in specific NAL and ENK binding in the olfactory bulb and thalamus+midbrain. In the hypothalamus, specific ENK binding was increased without any change in NAL binding. After the testosterone replacement in castrated rats, specific NAL binding was decreased and returned to the control level in the thalamus+midbrain, but remained high in the olfactory bulb. Specific ENK binding was decreased and returned to the control level in the olfactory bulb, hypothalamus and thalamus+midbrain. These results indicated that there are regional differences between u- and delta-type Op-R responses to castration and testosterone replacement. Op-R subtypes were regulated differentially by endogenous hormonal changes, such as testosterone.

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  • 老齢ラットにおけるNMDAレセプターの減少とBifemelane Hydrochloride投与による回復

    小川紀雄, 水川公直, 羽場久美子, 浅沼幹人

    Geriat. Med.(老年医学)   28 ( 12 )   1845 - 1849   1990.12

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  • Alterations of somatostatin and its modulation by levodopa in MPTP-treated mouse brain Reviewed

    Masato Asanuma, Norio Ogawa, Yukiko H. Sora, Khitisak Pongdhana, Kumiko Haba, Akitane Mori

    Journal of the Neurological Sciences   100 ( 1-2 )   155 - 160   1990.12

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    DOI: 10.1016/0022-510x(90)90027-k

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  • Effects of chronic administration of mergocryptine on changes in neurotransmitter levels in the ischemic gerbil brain. Reviewed

    Norio Ogawa, Kumiko Haba, Masato Asanuma, Mitsuhiro Kawata, Akitane Mori

    Archives Internationales de Pharmacodynamie et de Therapie   308 ( 1-2 )   21 - 31   1990.11

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    Changes in various neurotransmitter systems of the gerbil brain during ischemia and the effects of administration of mergocryptine, a new ergot derivative, were studied. Gerbils intraperitoneally administered 0.5 mg/kg of mergocryptine or the vehicle once a day for 14 days were used. The administration of mergocryptine to control animals had no effect on the contents of neurotransmitters or their metabolites in various regions of the brain, but it corrected abnormalities in the neurotransmitter systems caused by ischemia. These results suggest the usefulness of mergocryptine against the deleterious effects of brain ischemia.

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  • 塩酸フルナリジンの線条体D2ドーパミンレセプターに対する作用 Reviewed

    小川紀雄, 浅沼幹人, 高山晴彦, 佐藤博彦, 貫名 至

    臨床神経学   30 ( 11 )   1221 - 1226   1990.11

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  • Comparison of formaldehyde-preperfused frozen and freshly frozen tissue preparation for the in situ hybridization for alpha-tubulin messenger RNA in the rat brain Reviewed

    Masato Asanuma, Norio Ogawa, Kiminao Mizukawa, Kumiko Haba, Akitane Mori

    Research Communications in Chemical Pathology and Pharmacology   70 ( 2 )   183 - 192   1990.11

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  • ニューロトランスミッターとドプス-パーキンソン病治療薬としての基礎と臨床- Invited

    小川紀雄, 浅沼幹人

    薬の知識   41 ( 3 )   3 - 8   1990.3

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  • 老齢ラット脳におけるアセチルコリン系神経機構障害とnicergolineによる補正

    小川紀雄, 水川公直, 羽場久美子, 浅沼幹人

    Geriat. Med.(老年医学)   27 ( 8 )   1198 - 1204   1989.8

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Books

  • 生命金属ダイナミクス 生体内における金属の挙動と制御

    浅沼幹人, 宮崎育子( Role: Contributor ,  パーキンソン病と亜鉛結合蛋白. pp304-309)

    エヌ・ティー・エス,東京  2021 

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  • 脳内環境辞典

    浅沼幹人, 宮崎育子( Role: Contributor ,  Nrf2. pp122-123)

    メディカルドウ,大阪  2017 

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  • 脳内環境-維持機構と破綻がもたらす疾患研究

    浅沼幹人, 宮崎育子(アストロサイトの部位特異的プロファイルがもたらす脳内環境と神経保護.pp102-107)

    メディカルドウ,大阪  2014 

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  • 腎とフリーラジカル第10集

    浅沼幹人( Role: Contributor ,  酸化ストレスの評価のpitfall─神経科学からの話題.pp32-35)

    東京医学社,東京  2010 

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  • 実験薬理学 実践行動薬理学

    北村佳久, 浅沼幹人, 宮崎育子, 四宮一昭, 五味田裕( Role: Contributor ,  視床下部─下垂体─副腎皮質系過活動モデルを用いた治療抵抗性うつ病モデルの作製および創薬への応用. pp138-146)

    金芳堂,京都  2010 

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  • Handbook of Free Radicals: Formation, Types and Effects

    Ikuko Miyazaki, Masato Asanuma( Role: Contributor ,  Antioxidative and neuroprotective effects of metallothioneins on dopaminergic neurons. pp557-568)

    Nova Science Publishers, New York  2010 

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  • 酸化ストレス─フリーラジカル医学生物学の最前線 Ver.2

    宮崎育子, 浅沼幹人( Role: Contributor ,  カテコールアミン神経特異的酸化ストレスとしてのキノン体毒性とその防御. pp241-244)

    医歯薬出版,東京  2006 

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  • Immunosuppressant Analogs in Neuroprotection

    Ken-ichi Tanaka, Masato Asanuma, Norio Ogawa( Role: Contributor ,  Blockade of late-onset reduction of muscarinic acetylcholine receptors by immunosuppressants in forebrain ischemia. pp215-229)

    Humana Press, Totowa  2003 

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  • 酸化ストレス─フリーラジカル医学生物学の最前線

    浅沼幹人, 小川紀雄( Role: Contributor ,  酸化ストレスによる神経障害とその防御. pp177-181)

    医歯薬出版  2001 

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  • 脊髄小脳変性症の臨床

    浅沼幹人, 小川紀雄( Role: Contributor ,  脊髄小脳変性症の病態薬理化学. pp87-93)

    新興医学出版社  1999 

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  • Free radicals in brain physiology and disorders.

    Norio Ogawa, Emi Iwata, Masato Asanuma, Sakiko Nishibayashi, Kyoko Iida( Role: Contributor ,  Oxidative stress and transcription factors. pp131-140)

    Academic Press, San Diego  1996 

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  • 活性酸素とバイオシグナル

    浅沼幹人, 西林佐紀子, 小川紀雄( Role: Contributor ,  神経機能制御と活性酸素代謝. pp150-166.)

    講談社サイエンティフィック、東京  1996 

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  • 新しいSCDの臨床、脊髄小脳変性症の臨床

    小川紀雄, 浅沼幹人( Role: Contributor ,  脊髄小脳変性症の薬理化学的特徴と薬物治療. pp53-58)

    新興医学出版社、東京  1996 

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  • レセプター:基礎と臨床

    小川紀雄, 浅沼幹人( Role: Contributor ,  TRHレセプター, ソマトスタチンレセプター pp546-551)

    朝倉書店、東京  1993 

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  • 痴呆の基礎研究、高年期の痴呆シリーズ

    浅沼幹人, 小川紀雄( Role: Contributor ,  痴呆と神経伝達物質・レセプター. pp161-181)

    中央法規出版、東京  1993 

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  • Parkinson's Disease. From Aspects to Molecular Basis., Key Topics in Brain Research

    Norio Ogawa, Masato Asanuma( Role: Contributor ,  Receptor alterations in Parkinson's disease. pp39-51)

    Springer-Verlag, Wien  1991 

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  • Neuroreceptor Mechanisms in Brain

    Norio Ogawa, Kumiko Haba, Masato Asanuma, Kiminao Mizukawa, Akitane Mori( Role: Contributor ,  Super-delayed changes of muscarinic acetylcholine receptor in the gerbil hippocampus following transient ischemia. pp343-347)

    Plenum Publishing Corporation, New York  1991 

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MISC

  • メタロチオネイン欠損による脳梁形成不全の増悪

    正井加織, 菊岡 亮, 名越 武, 十川千春, 十川紀夫, 宮崎育子, 浅沼幹人

    日本解剖学会第75回中国・四国支部学術集会抄録集   2021.10

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  • アストロサイト−ミクログリア連関を介したロテノン誘発ドパミン神経障害へのメタロチオネインの関与

    宮崎育子, 菊岡 亮, 磯岡奈未, 村上真樹, 十川千春, 十川紀夫, 北村佳久, 浅沼幹人

    日本毒性学会生体金属部会メタルバイオサイエンス研究会2021抄録集   2021.10

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  • メタロチオネイン欠損マウスにおける脳梁形成不全

    正井加織, 菊岡 亮, 名越 武, 十川千春, 十川紀夫, 宮崎育子, 浅沼幹人

    日本毒性学会生体金属部会メタルバイオサイエンス研究会2021抄録集   2021.10

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  • LPS投与による機械的刺激反応閾値低下における金属結合タンパク質メタロチオネインの関与

    十川紀夫, 奥村雅代, 宮崎育子, 富田美穂子, 金銅英二, 十川千春, 浅沼幹人

    日本毒性学会生体金属部会メタルバイオサイエンス研究会2021抄録集   2021.10

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  • 妊娠・授乳期エポキシ樹脂BADGE曝露による新生仔マウス脳発達異常におけるエストロゲンβレセプターの関与

    浅沼幹人, 宮崎育子, 西山千春, 菊岡亮, 名越 武, Kyle Quin, 禅正和真

    第43回日本生物学的精神医学会・第51回日本神経精神薬理学会合同年会プログラム・抄録集   2021.7

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  • アストロサイト-ミクログリア連関がもたらす農薬ロテノン誘発ドパミン神経障害

    宮崎育子, 菊岡 亮, 磯岡奈未, 村上真樹, 十川千春, 十川紀夫, 北村佳久, 浅沼幹人

    第43回日本生物学的精神医学会・第51回日本神経精神薬理学会合同年会プログラム・抄録集   2021.7

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  • アストロサイトにおけるメタロチオネインを標的としたドパミン神経保護. シンポジウム: 生体金属部会シンポジウム 〜メタロチオネイン機能の新たな展開〜

    宮崎育子, 浅沼幹人

    第48回日本毒性学会学術年会抄録集   2021.7

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  • Rotenone-induced dopaminergic neurotoxicity mediated by astrocyte-microglia interaction

    Miyazaki, I, Kikuoka, R, Isooka, N, Murakami, S, Sogawa, C, Sogawa, N, Kitamura, Y, Asanuma, M

    第62回日本神経学会学術大会プログラム・抄録集   2021.5

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  • Involvement of estrogen receptor b in the abnormal brain development in fetuses by maternal bisphenol A diglycidyl ether exposure during gestation and lactation

    2021.3

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  • Astrocyte-microglia interaction promotes rotenone-induced dopaminergic neurotoxicity

    2021.3

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  • 5-HT1Aアゴニストによるアストロサイトのメタロチオネイン発現誘導とドパミン神経保護

    宮崎育子, 磯岡奈未, 菊岡 亮, 北村佳久, 浅沼幹人

    第14回パーキンソン病・運動障害疾患コングレス (MDSJ)プログラム・抄録集   2021.2

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  • ロテノン誘発ドパミン神経障害におけるアストロサイト−ミクログリア連関

    宮崎育子, 村上真樹, 菊岡 亮, 磯岡奈未, 十川千春, 十川紀夫, 北村佳久, 浅沼幹人

    日本毒性学会生体金属部会メタルバイオサイエンス研究会2020抄録集   2020.11

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  • パーキンソン病モデルマウスにおける杜仲抽出物のメタロチオネイン発現誘導および神経保護効果

    今福史智, Jin Sun, 磯岡奈未, 上舞 直, 清水崇司, 豊田俊明, 岡本裕成, 菊岡 亮, 宮崎育子, 浅沼幹人

    日本毒性学会生体金属部会メタルバイオサイエンス研究会2020抄録集   2020.11

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  • パーキンソン病と生体金属, 金属結合蛋白. シンポジウム: 生命金属で切り開く神経疾患の解明

    浅沼幹人

    第61回日本神経学会学術大会プログラム・抄録集   2020.9

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  • Region-specific glial dysfunction promotes rotenone neurotoxicity

    Miyazaki, I, Kikuoka, R, Isooka, N, Sogawa, C, Sogawa, N, Kitamura, Y, Asanuma, M

    第61回日本神経学会学術大会プログラム・抄録集   2020.8

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  • 農薬ロテノン曝露によるアストロサイトの部位特異的反応性の差異と神経細胞に及ぼす影響

    宮崎育子, 浅沼幹人, 村上真樹, 菊岡 亮, 磯岡奈未, 十川千春, 十川紀夫, 北村佳久

    第125回日本解剖学会総会抄録集   2020.3

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  • Glutathione in astrocytes as a target of neuroprotection.シンポジウム: 中枢神経におけるGSH産生促進を介する神経保護機構

    浅沼幹人

    第93回日本薬理学会年会抄録集   2020.3

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  • ロテノン投与パーキンソン病モデルにおけるコーヒー成分のメタロチオネイン発現誘導と神経保護効果

    磯岡奈未, 宮崎育子, 和田晃一, 菊岡 亮, 古川智英子, 北村佳久, 浅沼幹人

    日本毒性学会生体金属部会メタルバイオサイエンス研究会2019抄録集   2019.10

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  • ロテノン誘発部位特異的アストロサイト機能不全によるドパミン神経障害へのメタロチオネインの関与

    宮崎育子, 浅沼幹人, 村上真樹, 菊岡 亮, 磯岡奈未, 十川千春, 十川紀夫, 北村佳久

    日本毒性学会生体金属部会メタルバイオサイエンス研究会2019抄録集   2019.10

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  • 老齢メタロチオネインノックアウトマウスにおける脳組織学的変化

    菊岡 亮, 野村昌紀, 磯岡奈未, 宮崎育子, 十川紀夫, 十川千春, 北村佳久, 浅沼幹人

    日本毒性学会生体金属部会メタルバイオサイエンス研究会2019抄録集   2019.10

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  • Involvement of region-specific glial dysfunction in rotenone neurotoxicity

    Miyazaki, I, Asanuma, M, Murakami, S, Kikuoka, R, Isooka, N, Sogawa, C, Sogawa, N, Kitamura, Y

    VI AsCNP2019 Congress Abstract   2019.10

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  • ドパミン神経毒による酸化ストレスに対するアストロサイトの分子発現および神経保護作用の部位特異性

    浅沼 幹人, 奥村 菜央, 鳥越, 育子, 村上 真樹, 北村 佳久, 千堂 年昭

    第13回パーキンソン病・運動障害疾患コングレスプログラム・抄録集   13回   118 - 118   2019.7

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    Authorship:Lead author, Corresponding author   Language:Japanese   Publisher:Movement Disorder Society of Japan (MDSJ)  

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  • 部位特異的アストロサイト機能不全がもたらすロテノン誘発ドパミン神経障害

    宮崎 育子, 浅沼 幹人, 村上 真樹, 菊岡 亮, 磯岡 奈未, 十川 千春, 十川 紀夫, 北村 佳久

    第13回パーキンソン病・運動障害疾患コングレスプログラム・抄録集   13回   118 - 118   2019.7

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  • Regional differences in reaction of astrocytes against rotenone contribute to dopaminergic neurodegeneration

    Miyazaki, I, Asanuma, M, Murakami, S, Kikuoka, R, Isooka, N, Sogawa, C, Sogawa, N, Kitamura, Y

    14th European Meeting on Glial Cells in Health and Disease Congress Abstract   2019.7

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  • Region-specific features of astrocytes against dopaminergic neurotoxin-induced oxidative stress

    Asanuma, M, Okumura-Torigoe, N, Miyazaki, I, Murakami, S, Kitamura, Y, Sendo, T

    14th European Meeting on Glial Cells in Health and Disease Congress Abstract   2019.7

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  • 妊娠・授乳期のエポキシ樹脂曝露が新生仔マウスに及ぼす行動毒性

    宮崎育子, 菊岡 亮, 磯岡奈未, 禅正和真, 新居 麗, 園部奏生, 船越英丸, 中山恵利香, 進 浩太郎, 山本大地, Kyle Quin, 浅沼幹人

    第46回日本毒性学会学術年会抄録集   2019.6

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  • Rotigotine protects dopaminergic neurons via astrocytic serotonin 1A receptors

    Miyazaki, I, Isooka, N, Kikuoka, R, Wada, K, Nakayama, E, Shin, K, Yamamoto, D, Kitamura, Y, Asanuma, M

    2019.5

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  • 妊娠・授乳期にエポキシ樹脂曝露した新生仔マウスの脳発達に関する組織学的・行動学的解析

    宮崎育子, 菊岡 亮, 磯岡奈未, 禅正和真, 新居 麗, 園部奏生, 船越英丸, 中山恵利香, 進 浩太郎, 山本大地, Kyle Quin, 浅沼幹人

    第124回日本解剖学会総会抄録集   2019.3

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  • Treatment with coffee ingredients protects central and myenteric neurons in parkinsonian model

    Miyazaki, I, Isooka, N, Wada, K, Kikuoka, R, Kitamura, Y, Asanuma, M

    2019.3

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  • 大学院生が期待するウェットからドライな薬学研究の未来 抗がん剤投与による不安症状の発症機序解明とその治療・予防に向けたアプローチ

    住吉 佑介, 内藤 七海, 中村 優花, 菅 詩歩, 牛尾 聡一郎, 宮崎 育子, 浅沼 幹人, 北村 佳久, 千堂 年昭

    日本薬学会年会要旨集   139年会 ( 1 )   329 - 329   2019.3

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  • ロチゴチンによるアストロサイトのセロトニン1Aレセプターを標的としたドパミン神経保護

    宮崎 育子, 磯岡 奈未, 菊岡 亮, 和田 晃一, 中山 恵利香, 進 浩太郎, 山本 大地, 北村 佳久, 浅沼 幹人

    パーキンソン病・運動障害疾患コングレスプログラム・抄録集   12回   117 - 117   2018.7

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  • 医療のさらなる安心・安全を志向する若手研究者のイノベーティブチャレンジ 抗がん剤投与による不安症状発症の病態機序解明 セロトニン神経系の関与

    中村 優花, 住吉 佑介, 内藤 七海, 牛尾 聡一郎, 宮崎 育子, 浅沼 幹人, 北村 佳久, 千堂 年昭

    日本薬学会年会要旨集   138年会 ( 1 )   333 - 333   2018.3

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  • 医療のさらなる安心・安全を志向する若手研究者のイノベーティブチャレンジ 抗がん剤投与による不安症状発症の病態機序解明 セロトニン神経系の関与

    中村 優花, 住吉 佑介, 内藤 七海, 牛尾 聡一郎, 宮崎 育子, 浅沼 幹人, 北村 佳久, 千堂 年昭

    日本薬学会年会要旨集   138年会 ( 1 )   333 - 333   2018.3

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  • Behavioral analysis of single prolonged stress-induced anxiety-related behaviors in mice

    TANAKA Ken-ichi, TANAKA Ken-ichi, YAGI Takao, YAGI Takao, ASANUMA Masato

    Journal of Physiological Sciences   68 ( Supplement 1 )   2018

  • 農薬ロテノン暴露による腸管神経障害とコーヒー成分による神経保護効果

    宮崎 育子, 磯岡 奈未, 菊岡 亮, 和田 晃一, 北村 佳久, 浅沼 幹人

    パーキンソン病・運動障害疾患コングレスプログラム・抄録集   11回   99 - 99   2017.10

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  • 農薬ロテノンによるアストロサイト機能異常がもたらすドパミン神経障害

    宮崎 育子, 菊岡 亮, 磯岡 奈未, 北村 佳久, 浅沼 幹人

    日本生物学的精神医学会・日本神経精神薬理学会合同年会プログラム・抄録集   39回・47回   158 - 158   2017.9

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    Language:Japanese   Publisher:日本生物学的精神医学会・日本神経精神薬理学会  

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  • アストロサイトを介したミルタザピンのドパミン神経保護効果に関する検討

    菊岡 亮, 宮崎 育子, 久保田 菜月, 前田 恵実, 香川 大樹, 守山 雅晃, 粂 明日香, 北村 佳久, 浅沼 幹人

    日本生物学的精神医学会・日本神経精神薬理学会合同年会プログラム・抄録集   39回・47回   193 - 193   2017.9

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  • 農薬ロテノンによる非細胞自律性ドパミン神経障害

    宮崎 育子, 村上 真樹, 菊岡 亮, 磯岡 奈未, 北村 佳久, 浅沼 幹人

    The Journal of Toxicological Sciences   42 ( Suppl. )   S321 - S321   2017.6

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  • 革新的創薬・育薬を目指す若手研究者によるトランスレーショナルリサーチの最前線 パーキンソン病モデルマウスにおけるミルタザピンの神経保護効果に関する検討

    菊岡 亮, 宮崎 育子, 浅沼 幹人, 北村 佳久, 千堂 年昭

    日本薬学会年会要旨集   137年会 ( 1 )   284 - 284   2017.3

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  • ALSモデルの運動障害および運動神経変性に対するセロトニン1Aアゴニストの抑制効果

    浅沼幹人, 宮崎育子, 村上真樹, 村上真樹, 鳥越菜央, 中野剛志, 菊岡亮, 北村佳久, 千堂年昭

    パーキンソン病・運動障害疾患コングレスプログラム・抄録集   10th   68 - 68   2016.10

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  • 農薬ロテノン暴露によるドパミン神経障害におけるアストロサイトの関与

    宮崎育子, 村上真樹, 村上真樹, 菊岡亮, 磯岡奈未, 北村佳久, 浅沼幹人

    パーキンソン病・運動障害疾患コングレスプログラム・抄録集   10th   69 - 69   2016.10

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  • パーキンソン病モデルマウスにおけるミルタザピンの神経保護効果に関する検討(Neuroprotective effects of mirtazapine in parkinsonian mice)

    菊岡 亮, 宮崎 育子, 久保田 菜月, 前田 恵実, 香川 大樹, 守山 雅晃, 粂 明日香, 村上 真樹, 北村 佳久, 浅沼 幹人

    日本神経精神薬理学会年会プログラム・抄録集   46回   232 - 232   2016.7

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  • 抗うつ薬ミルタザピンのアストロサイトを標的としたドパミン神経保護(Astrocyte-targeted neuroprotection of antidepressant mirtazapine)

    宮崎 育子, 菊岡 亮, 久保田 菜月, 前田 恵実, 香川 大樹, 守山 雅晃, 粂 明日香, 村上 真樹, 北村 佳久, 浅沼 幹人

    日本神経精神薬理学会年会プログラム・抄録集   46回   232 - 232   2016.7

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  • 筋萎縮性側索硬化症モデルにおける運動障害および運動神経変性に対する8-OH-DPATの抑制効果(8-OH-DPAT ameliorates motor dysfunction and motor neuron degeneration in mouse model of amyotrophic lateral sclerosis)

    浅沼 幹人, 宮崎 育子, 村上 真樹, 鳥越 奈央, 中野 剛志, 菊岡 亮, 北村 佳久, 千堂 年昭

    日本神経精神薬理学会年会プログラム・抄録集   46回   232 - 232   2016.7

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  • パーキンソン病モデルマウスにおけるアストロサイトの5‐HT1Aレセプターを標的とした神経保護

    宮崎育子, 宮崎育子, 菊岡亮, 久保田菜月, 前田恵実, 香川大樹, 村上真樹, 村上真樹, 北村佳久, 浅沼幹人, 浅沼幹人

    パーキンソン病・運動障害疾患コングレスプログラム・抄録集   9th   67 - 67   2015.10

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  • ミルタザピンのアストロサイトを標的としたドパミン神経保護効果

    宮崎育子, 菊岡亮, 久保田菜月, 前田恵実, 香川大樹, 村上真樹, 村上真樹, 北村佳久, 浅沼幹人, 浅沼幹人

    日本神経精神薬理学会プログラム・抄録集   45th   185 - 185   2015.9

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  • ALSモデルマウスにおけるセロトニン1Aアゴニストによる神経保護効果の検討

    中野剛志, 鳥越菜央, 村上真樹, 宮崎育子, 浅沼幹人, 北村佳久, 千堂年昭

    日本薬学会年会要旨集(CD-ROM)   135th ( 3 )   ROMBUNNO.28PB-PM242 - 191   2015.3

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  • アストロサイトを介したレベチラセタムのドパミン神経保護効果に関する検討

    宮崎育子, 村上真樹, 鳥越菜央, 北村佳久, 浅沼幹人

    日本薬理学会近畿部会プログラム・要旨集   125th   37   2014.5

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  • ACTH反復投与ラットにおけるketamineの抗うつ効果に関する検討

    中村紘子, 米田紗緒里, 野白有里子, 宮崎育子, 浅沼幹人, 北村佳久, 千堂年昭

    日本薬学会年会要旨集(CD-ROM)   134th ( 3 )   ROMBUNNO.28PMM-105 - 151   2014.3

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  • Neuroprotective effects of levetiracetam in parkinsonian model mice

    Ikuko Miyazaki, Shinki Murakami, Nao Torigoe, Yoshihisa Kitamura, Masato Asanuma

    JOURNAL OF PHARMACOLOGICAL SCIENCES   124   150P - 150P   2014

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  • ALSモデルマウスにおけるセロトニン1Aアゴニストによる神経保護効果の検討

    中野剛志, 鳥越菜央, 村上真樹, 宮崎育子, 浅沼幹人, 北村佳久, 千堂年昭

    日本生物学的精神医学会誌   154   2014

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  • 抗がん剤投与ラットにおける精神機能および海馬神経新生に関する検討

    米田紗緒里, 服部紗代, 中村紘子, 宮崎育子, 浅沼幹人, 北村佳久, 千堂年昭

    日本薬学会年会要旨集(CD-ROM)   134th   ROMBUNNO.GS02-7   2014

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  • 線条体アストロサイトが酸化ストレスに対して発現誘導する因子の網羅的解析

    鳥越 菜央, 宮崎 育子, 村上 真樹, 北村 佳久, 千堂 年昭, 浅沼 幹人

    日本臨床精神神経薬理学会・日本神経精神薬理学会合同年会プログラム・抄録集   23回・43回   250 - 250   2013.10

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  • セロトニン1Aアゴニストによるアストロサイトにおけるメタロチオネイン発現誘導とドパミン神経保護

    宮崎 育子, 村上 真樹, 竹島 美香, 鳥越 菜央, 三好 耕, 北村 佳久, 浅沼 幹人

    日本臨床精神神経薬理学会・日本神経精神薬理学会合同年会プログラム・抄録集   23回・43回   251 - 251   2013.10

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  • ラットの行動変化から推察する抗がん剤投与による精神機能変化―ドキソルビシンおよびシクロホスファミド投与による影響―

    北村佳久, 服部紗代, 米田沙緒里, 三宅彩香, 小山敏広, 宮崎育子, 浅沼幹人, 千堂年昭

    日本サイコオンコロジー学会総会プログラム・抄録集   26th   132   2013

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  • Neuroprotective effects of serotonin-1a agonist 8-OH-DPAT in parkinsonian mice

    Ikuko Miyazaki, Shinki Murakami, Mika Takeshima, Masato Asanuma

    JOURNAL OF PHARMACOLOGICAL SCIENCES   118   111P - 111P   2012

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  • ACTH反復投与ラットにおける海馬細胞新生の減少およびそのメカニズムに関する検討

    林宏美, 土居真穂, 尾上由華, 鍬塚圭子, 三宅彩香, 小山敏広, 四宮一昭, 宮崎育子, 浅沼幹人, 北村佳久

    日本薬学会年会要旨集   131st ( 1 )   257   2011.3

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  • Effects of imipramine and lithium on the suppression of cell proliferation in the dentate gyrus of the hippocampus in ACTH treated rats

    Hiromi Hayashi, Maho Doi, Yuka Onoue, Keiko Kuwatsuka, Ayaka Miyake, Toshihiro Koyama, Kazuaki Shinomiya, Ikuko Miyazaki, Masato Asanuma, Yoshihisa Kitamura

    JOURNAL OF PHARMACOLOGICAL SCIENCES   115   251P - 251P   2011

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  • Dopamine receptors localize to the neuronal primary cilium, a non-synaptic neurotransmission device

    Ko Miyoshi, Kyosuke Kasahara, Shinki Murakami, Ikuko Miyazaki, Masato Asanuma

    NEUROSCIENCE RESEARCH   71   E87 - E87   2011

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    DOI: 10.1016/j.neures.2011.07.372

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  • Effects of rotenone exposure on primary cultured enteric neuronal or glial cells

    Ikuko Miyazaki, Shinki Murakami, Mika Takeshima, Ko Miyoshi, Masato Asanuma

    NEUROSCIENCE RESEARCH   71   E190 - E190   2011

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    DOI: 10.1016/j.neures.2011.07.820

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  • Effects of chronic rotenone exposure on enteric neuronal or glial cells in vivo

    Shinki Murakami, Ikuko Miyazaki, Mika Takeshima, Ko Miyoshi, Masato Asanuma

    NEUROSCIENCE RESEARCH   71   E190 - E190   2011

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    DOI: 10.1016/j.neures.2011.07.821

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  • Reply to Ahmad Ghanizadeh, A Novel Hypothesized Clinical Implication of Zonisamide for Autism. Reviewed

    Masato Asanuma, Ikuko Miyazaki

    Annals of Neurology   69 ( 2 )   426 - 427   2011

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  • アストロサイトの抗酸化防御機構を標的とした神経保護.

    浅沼幹人

    日本脳神経外科学会第68回学術総会ランチョンセミナー Congress Report   2010

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  • Effects of docosahexaenoic acid on methamphetamine-induced neurotoxicity in cultured dopaminergic neuronal cells

    Maiko Murata, Natsuho Urasoe, Ikuko Miyazaki, Masato Asanuma, Taizo Kita

    JOURNAL OF PHARMACOLOGICAL SCIENCES   112   139P - 139P   2010

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  • Morphine単回投与ラットにおけるnaloxone誘発条件付け場所嫌悪行動に対する扁桃体中心核内α7ニコチン受容体の関与

    石田茂, 河崎陽一, 浅沼幹人, 松永尚, 千堂年昭, 荒木博陽, 川崎博己, 北村佳久

    日本薬理学会近畿部会プログラム・要旨集   117th   25   2010

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  • Morphine単回投与ラットのnaloxone誘発退薬行動に対するnicotineの効果における扁桃体の関与

    石田茂, 河崎陽一, 浅沼幹人, 松永尚, 千堂年昭, 荒木博陽, 川崎博己, 北村佳久

    日本臨床精神神経薬理学会・日本神経精神薬理学会合同年会プログラム・抄録集   20th-40th   167   2010

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  • Dopamine-specific metallothionein induction in reactive astrocytes through dopamine transporter

    Ikuko Miyazaki, Yuri Kikkawa, Mika Takeshima, Masato Asanuma

    JOURNAL OF PHARMACOLOGICAL SCIENCES   112   91P - 91P   2010

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  • Astrocytes protect dopaminergic neurons from dopamine quinone toxicity

    Ikuko Miyazaki, Yuri Kikkawa, Mika Takeshima, Ko Miyoshi, Taizo Kita, Masato Asanuma

    NEUROSCIENCE RESEARCH   68   E347 - E347   2010

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    DOI: 10.1016/j.neures.2010.07.1537

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  • L-theanine up-regulates glutathione levels in astrocytes and protects excess dopamine-induced neurotoxicity

    Mika Takeshima, Ikuko Miyazaki, Yuri Kikkawa, Taizo Kita, Masato Asanuma

    JOURNAL OF PHARMACOLOGICAL SCIENCES   112   54P - 54P   2010

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  • Lithium elongates neuronal primary cilia

    Ko Miyoshi, Kyosuke Kasahara, Ikuko Miyazaki, Masato Asanuma

    NEUROSCIENCE RESEARCH   68   E84 - E84   2010

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    DOI: 10.1016/j.neures.2010.07.138

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  • 杜仲葉含有成分クロロゲン酸およびその代謝物の精神機能へ及ぼす影響

    四宮一昭, 松永康臣, 浅沼幹人, 千堂年昭, 川崎博己, 北村佳久

    日本杜仲研究会定期大会講演要旨集   4th   29   2009.7

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  • メタンフェタミン神経毒性に対するインターフェロンγおよびPPARγアゴニストの保護効果(Protective effects of interferon-γ or peroxisome proliferator-activated receptor-γ agonist against methamphetamine-induced neurotoxicity)

    浅沼 幹人, 宮崎 育子, 福岡 早紀, 穂積 宏彰, 辻 武史, 北村 佳久, 千堂 年昭, 喜多 大三

    神経化学   48 ( 2-3 )   214 - 214   2009.6

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  • Effects of docosahexaenoic acid on dopaminergic neuronal cells

    Maiko Murata, Mika Takeshima, Megumi Someya, Ikuko Miyazaki, Masato Asanuma, Taizo Kita

    JOURNAL OF PHARMACOLOGICAL SCIENCES   109   278P - 278P   2009

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  • Studies on drug dependence (Rept.436): Distinct mechanism of methamphetamine- and methylphenidate-induced dopaminergic neurotoxicity

    Daigo Ikegami, Minoru Narita, Megumi Asato, Yuri Tsurukawa, Keiichi Niikura, Michiko Narita, Masato Asanuma, Taizo Kita, Naoko Kuzumaki, Tsutomu Suzuki

    JOURNAL OF PHARMACOLOGICAL SCIENCES   109   95P - 95P   2009

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  • Effects of L-theanine on dopaminergic neuronal cells

    Megumi Someya, Mika Takeshima, Maiko Murata, Ikuko Miyazaki, Masato Asanuma, Taizo Kita

    JOURNAL OF PHARMACOLOGICAL SCIENCES   109   277P - 277P   2009

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  • Reactive astrocyte-specific induction of metallothionein in methamphetamine-induced neurotoxicity

    Ikuko Miyazaki, Yuri Kikkawa, Mika Takeshima, Ko Miyoshi, Taizo Kita, Masato Asanuma

    NEUROSCIENCE RESEARCH   65   S256 - S256   2009

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    DOI: 10.1016/j.neures.2009.09.1458

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  • Cyclooxygenase-independent neuroprotective effects of aspirin against dopamine quinone-induced neurotoxicity

    Yuri Kikkawa, Naotaka Kimoto, Saki Fukuoka, Ikuko Miyazaki, Masato Asanuma

    JOURNAL OF PHARMACOLOGICAL SCIENCES   109   279P - 279P   2009

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  • Analysis of mice carrying a 129 substrain-derived deletion variant in Disc1

    Ko Miyoshi, Kyosuke Kasahara, Ikuko Miyazaki, Masato Asanuma

    NEUROSCIENCE RESEARCH   65   S122 - S122   2009

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    DOI: 10.1016/j.neures.2009.09.577

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  • 精神疾患改善薬スクリーニングモデル動物を用いたローヤルゼリーの薬効評価

    八木貴彦, 松永康臣, 江角悟, 四宮一昭, 千堂年昭, 浅沼幹人, 北村佳久

    日本臨床精神神経薬理学会・日本神経精神薬理学会合同年会プログラム・抄録集   19th-39th   247   2009

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  • メタンフェタミン急性神経毒性に対するインターフェロン‐γの保護効果発現機序に関する検討

    福岡早紀, 浅沼幹人, 宮崎育子, 穂積宏彰, 吉川友理, 木本直孝, 北村佳久, 千堂年昭, 喜多大三

    日本薬理学雑誌   132 ( 3 )   16P   2008.9

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  • メタンフェタミン神経毒性に対するインターフェロンγの保護効果におけるペルオキシソーム増殖剤活性化受容体γ(PPARγ)の関与(Possible involvement of peroxisome proliferator-activated receptor-γ in protective effects of interferon-γ against methamphetamine-induced neurotoxicity)

    浅沼 幹人, 福岡 早紀, 穂積 宏彰, 宮崎 育子, 北村 佳久, 千堂 年昭, 喜多 大三

    神経化学   47 ( 2-3 )   237 - 237   2008.8

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  • Biological roles for neuronal primary cilia

    K. Miyoshi, I. Miyazaki, M. Asanuma

    PSYCHIATRY AND CLINICAL NEUROSCIENCES   62 ( 1 )   S6 - S6   2008.2

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  • Protective effects of interferon-gamma against methamphetamine-induced neurotoxicity

    Hiroaki Hozumi, Masato Asanuma, Ikuko Miyazaki, Saki Fukuoka, Yuri Kikkawa, Naotaka Kimoto, Yoshihisa Kitamura, Toshiaki Sendou, Taizou Kita, Yutaka Gomita

    JOURNAL OF PHARMACOLOGICAL SCIENCES   106   175P - 175P   2008

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  • Functional analysis of neuronal cilia using pericentrin mutant mice

    Ko Miyoshi, Kyosuke Kasahara, Ikuko Miyazaki, Masato Asanuma

    NEUROSCIENCE RESEARCH   61   S207 - S207   2008

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  • Effect of baicalin, flavone glucuronide on dopaminergic neuronal cells

    Mika Takeshirna, Yumiko Tanaka, Megurni Someya, Maiko Murata, Ikuko Miyazaki, Masato Asanuma

    JOURNAL OF PHARMACOLOGICAL SCIENCES   106   93P - 93P   2008

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  • メタンフェタミン急性神経毒性に対するインターフェロン‐γの保護効果発現機序に関する検討

    福岡早紀, 浅沼幹人, 宮崎育子, 穂積宏彰, 吉川友理, 木本直孝, 北村佳久, 千堂年昭, 喜多大三

    日本薬理学会近畿部会プログラム・要旨集   113rd   38   2008

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  • Expression profiling of inflammatory molecules related to methamphetamine-induced neurotoxicity

    27 ( 5 )   2007.11

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  • メチルフェニデートのドパミン神経毒性に対する作用

    日名俊行, 浅沼幹人, 喜多大三, 宮崎育子, 小川紀雄, 北村佳久, 千堂年昭, 五味田裕

    日本薬学会年会要旨集   127th ( 2 )   129   2007.3

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  • Functional analysis of neuronal primary cilia using pericentrin mutant mice

    Ko Miyoshi, Ikuko Miyazaki, Masato Asanuma

    NEUROSCIENCE RESEARCH   58   S123 - S123   2007

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  • Specific expression of proapoptotic factor PAG608 on motor neurons in spinal cords of L-DOPA-treated parkinsonian models

    Ikuko Miyazaki, Masako Shimizu, Francisco J. Diaz-Corrales, Maria F. Esraba-Alba, Masato Asanuma

    NEUROSCIENCE RESEARCH   55   S201 - S201   2006

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  • Pericentrin is localized to the base of neuronal primary cilia in the developing cerebral cortex

    Ko Miyoshi, Ikuko Miyazaki, Masato Asanuma

    NEUROSCIENCE RESEARCH   55   S233 - S233   2006

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  • Aggregation of parkin protein in the centrosome and accumulation of cyclin E/cdk 2 complex in CATH.a cells treated with dopamine

    F. J. Diaz-Corrales, M. Asanuma, I. Miyazaki, K. Miyoshi, N. Ogawa

    MOVEMENT DISORDERS   21   S580 - S581   2006

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  • Dopamine agonist pergolide prevents levodopa-induced quinoprotein formation in parkinsonian striatum and shows quenching effects on dopamine-semiquinone generated in vitro

    N Ogawa, M Asanuma, L Miyazaki, FJ Diaz-Corrales

    MOVEMENT DISORDERS   20   S69 - S69   2005

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    DOI: 10.1097/01.wnf.0000175523.33334.24

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  • 心不全における酸化ストレスの関与-基礎的ならびに臨床的検討 Invited

    中村一文, 草野研吾, 垣下幹夫, 三浦 綾, 久松研一, 西井伸洋, 伴場主一, 渡辺敦之, 藤尾栄起, 宮地克維, 永瀬 聡, 森田 宏, 斎藤博則, 江森哲郎, 浅沼幹人, 宮崎正博, 中村陽一, 松原広己, 大江 透

    岡山医学会雑誌   116   9 - 16   2004

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  • マンガン誘発神経毒性におけるパーキン蛋白のドパミン神経特異的な関与

    宮崎 育子, 浅沼 幹人, 東 洋一郎, 服部 信孝, 水野 美邦, 小川 紀雄

    日本神経精神薬理学雑誌 = Japanese journal of psychopharmacology   23 ( 6 )   2003.12

  • メタンフェタミン神経毒性におけるp53関連遺伝子の関与

    浅沼 幹人, 東 洋一郎, 宮崎 育子, 辻 武史, 田中 健一, 小川 紀雄

    日本神経精神薬理学雑誌 = Japanese journal of psychopharmacology   21 ( 6 )   311 - 311   2001.12

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  • 非免疫抑制性イムノフィリンリガンドの神経保護効果とその分子機序

    田中 健一, 吉岡 真世, 藤田 尚子, 浅沼 幹人, 小川 紀雄

    日本神経精神薬理学雑誌 = Japanese journal of psychopharmacology   21 ( 6 )   304 - 304   2001.12

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Presentations

  • LPS投与による機械的刺激反応閾値低下における金属結合タンパク質メタロチオネインの関与

    十川紀夫, 奥村雅代, 宮崎育子, 富田美穂子, 金銅英二, 十川千春, 浅沼幹人

    日本毒性学会生体金属部会メタルバイオサイエンス研究会2021  2021.10.27 

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    Event date: 2021.10.27 - 2021.10.28

    Language:Japanese   Presentation type:Poster presentation  

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  • アストロサイト−ミクログリア連関を介したロテノン誘発ドパミン神経障害へのメタロチオネインの関与

    宮崎育子, 菊岡 亮, 磯岡奈未, 村上真樹, 十川千春, 十川紀夫, 北村佳久, 浅沼幹人

    日本毒性学会生体金属部会メタルバイオサイエンス研究会2021  2021.10.27 

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    Event date: 2021.10.27 - 2021.10.28

    Language:Japanese   Presentation type:Oral presentation (general)  

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  • メタロチオネイン欠損マウスにおける脳梁形成不全

    正井加織, 菊岡 亮, 名越 武, 十川千春, 十川紀夫, 宮崎育子, 浅沼幹人

    日本毒性学会生体金属部会メタルバイオサイエンス研究会2021  2021.10.27 

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    Event date: 2021.10.27 - 2021.10.28

    Language:Japanese   Presentation type:Poster presentation  

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  • 妊娠・授乳期エポキシ樹脂BADGE曝露による新生仔マウス脳発達異常におけるエストロゲンβレセプターの関与.

    浅沼幹人, 宮崎育子, 西山千春, 菊岡亮, 名越 武, Kyle Quin, 禅正和真

    第43回日本生物学的精神医学会・第51回日本神経精神薬理学会合同年会  2021.7.14 

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    Event date: 2021.7.14 - 2021.7.16

    Language:Japanese   Presentation type:Oral presentation (general)  

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  • アストロサイト-ミクログリア連関がもたらす農薬ロテノン誘発ドパミン神経障害.

    宮崎育子, 菊岡 亮, 磯岡奈未, 村上真樹, 十川千春, 十川紀夫, 北村佳久, 浅沼幹人

    第43回日本生物学的精神医学会・第51回日本神経精神薬理学会合同年会  2021.7.14 

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    Event date: 2021.7.14 - 2021.7.16

    Language:Japanese   Presentation type:Poster presentation  

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  • Rotenone-induced dopaminergic neurotoxicity mediated by astrocyte-microglia interaction.

    Miyazaki, I, Kikuoka, R, Isooka, N, Murakami, S, Sogawa, C, Sogawa, N, Kitamura, Y, Asanuma, M

    第62回日本神経学会学術大会  2021.5.19 

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    Event date: 2021.5.19 - 2021.5.22

    Language:English   Presentation type:Poster presentation  

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  • 妊娠・授乳期エポキシ樹脂曝露による新生仔マウスの脳発達異常へのエストロゲン受容体βの関与.

    宮崎育子, 西山千春, 菊岡 亮, 名越 武, Kyle Quin, 磯岡奈未, 禅正和真, 浅沼幹人

    第126回日本解剖学会総会  2021.3.28 

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    Event date: 2021.3.28 - 2021.3.30

    Language:Japanese   Presentation type:Poster presentation  

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  • アストロサイト−ミクログリア連関がもたらすロテノン誘発ドパミン神経障害.

    宮崎育子, 菊岡 亮, 磯岡奈未, 十川千春, 十川紀夫, 北村佳久, 浅沼幹人

    第94回日本薬理学会年会  2021.3.8 

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    Event date: 2021.3.8 - 2021.3.10

    Language:Japanese   Presentation type:Oral presentation (general)  

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  • 5-HT1Aアゴニストによるアストロサイトのメタロチオネイン発現誘導とドパミン神経保護.

    宮崎育子, 磯岡奈未, 菊岡 亮, 北村佳久, 浅沼幹人

    第14回パーキンソン病・運動障害疾患コングレス (MDSJ)  2021.2.22 

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    Event date: 2021.2.22 - 2021.2.24

    Language:Japanese   Presentation type:Poster presentation  

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  • ロテノン誘発ドパミン神経障害におけるアストロサイト−ミクログリア連関.

    宮崎育子, 村上真樹, 菊岡 亮, 磯岡奈未, 十川千春, 十川紀夫, 北村佳久, 浅沼幹人

    日本毒性学会生体金属部会メタルバイオサイエンス研究会2020  2020.11.6 

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    Event date: 2020.11.6 - 2020.11.7

    Language:Japanese   Presentation type:Oral presentation (general)  

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  • パーキンソン病モデルマウスにおける杜仲抽出物のメタロチオネイン発現誘導および神経保護効果.

    今福史智, Jin Sun, 磯岡奈未, 上舞 直, 清水崇司, 豊田俊明, 岡本裕成, 菊岡 亮, 宮崎育子, 浅沼幹人

    日本毒性学会生体金属部会メタルバイオサイエンス研究会2020  2020.11.6 

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    Event date: 2020.11.6 - 2020.11.7

    Language:Japanese   Presentation type:Poster presentation  

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  • Region-specific glial dysfunction promotes rotenone neurotoxicity.

    Miyazaki, I, Kikuoka, R, Isooka, N, Sogawa, C, Sogawa, N, Kitamura, Y, Asanuma, M

    第61回日本神経学会学術大会  2020.8.31 

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    Event date: 2020.8.31 - 2020.9.2

    Language:English   Presentation type:Poster presentation  

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  • ロチゴチンのアストロサイトセロトニン1A受容体を標的としたド パミン神経保護効果.

    磯岡 奈未, 宮崎 育子, 菊岡 亮, 和田 晃一, 中山 恵利香, 進 浩太郎, 山本 大地, 北村 佳久, 浅沼 幹人

    第32回創薬・薬理フォーラム岡山  2019.12.21 

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    Event date: 2019.12.21

    Language:Japanese   Presentation type:Oral presentation (general)  

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  • 神経毒によるドパミン神経障害における部位特異的神経-グリア連関.

    浅沼幹人, 磯岡奈未, 菊岡亮, 宮崎育子

    第17回神経科学研究会  2019.11.23 

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    Event date: 2019.11.23

    Language:Japanese   Presentation type:Oral presentation (general)  

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  • ロテノン誘発部位特異的アストロサイト機能不全によるドパミン神経障害へのメタロチオネインの関与.

    宮崎育子, 浅沼幹人, 村上真樹, 菊岡 亮, 磯岡奈未, 十川千春, 十川紀夫, 北村佳久

    日本毒性学会生体金属部会メタルバイオサイエンス研究会2019  2019.10.30 

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    Event date: 2019.10.30

    Language:Japanese   Presentation type:Oral presentation (general)  

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  • ロテノン投与パーキンソン病モデルにおけるコーヒー成分のメタロチオネイン発現誘導と神経保護効果.

    磯岡奈未, 宮崎育子, 和田晃一, 菊岡 亮, 古川智英子, 北村佳久, 浅沼幹人

    日本毒性学会生体金属部会メタルバイオサイエンス研究会2019  2019.10.30 

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    Event date: 2019.10.30

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  • 老齢メタロチオネインノックアウトマウスにおける脳組織学的変化.

    菊岡 亮, 野村昌紀, 磯岡奈未, 宮崎育子, 十川紀夫, 十川千春, 北村佳久, 浅沼幹人

    日本毒性学会生体金属部会メタルバイオサイエンス研究会2019  2019.10.29 

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    Event date: 2019.10.29

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  • Involvement of region-specific glial dysfunction in rotenone neurotoxicity.

    Miyazaki, I, Asanuma, M, Murakami, S, Kikuoka, R, Isooka, N, Sogawa, C, Sogawa, N, Kitamura, Y

    VI AsCNP2019  2019.10.11 

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    Event date: 2019.10.11 - 2019.10.13

    Language:English   Presentation type:Poster presentation  

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  • 抗うつ薬ミルタザピンの神経−グリア連関を介したドパミン神経保護作用.

    菊岡 亮, 宮崎育子, 村上真樹, 北村佳久, 千堂年昭, 浅沼幹人

    第31回創薬・薬理フォーラム岡山  2019.7.27 

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    Event date: 2019.7.27

    Language:Japanese   Presentation type:Oral presentation (general)  

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  • 部位特異的アストロサイト機能不全がもたらすロテノン誘発ドパミン神経障害.

    宮崎育子, 浅沼幹人, 村上真樹, 菊岡 亮, 磯岡奈未, 十川千春, 十川紀夫, 北村佳久

    第13回パーキンソン病・運動障害疾患コングレス (MDSJ)  2019.7.25 

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    Event date: 2019.7.25 - 2019.7.27

    Language:Japanese   Presentation type:Poster presentation  

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  • ドパミン神経毒による酸化ストレスに対するアストロサイトの分子発現および神経保護作用の部位特異性.

    浅沼幹人, 奥村, 鳥越, 菜央, 宮崎育子, 村上真樹, 北村佳久, 千堂年昭

    第13回パーキンソン病・運動障害疾患コングレス (MDSJ)  2019.7.25 

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    Event date: 2019.7.25 - 2019.7.27

    Language:Japanese   Presentation type:Poster presentation  

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  • Regional differences in reaction of astrocytes against rotenone contribute to dopaminergic neurodegeneration.

    Miyazaki, I, Asanuma, M, Murakami, S, Kikuoka, R, Isooka, N, Sogawa, C, Sogawa, N, Kitamura, Y

    14th European Meeting on Glial Cells in Health and Disease  2019.7.10 

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    Event date: 2019.7.10 - 2019.7.13

    Language:English   Presentation type:Poster presentation  

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  • Region-specific features of astrocytes against dopaminergic neurotoxin-induced oxidative stress.

    Asanuma, M, Okumura-Torigoe, N, Miyazaki, I, Murakami, S, Kitamura, Y, Sendo, T

    14th European Meeting on Glial Cells in Health and Disease  2019.7.10 

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    Event date: 2019.7.10 - 2019.7.13

    Language:English   Presentation type:Poster presentation  

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  • 妊娠・授乳期のエポキシ樹脂曝露が新生仔マウスに及ぼす行動毒性.

    宮崎育子, 菊岡 亮, 磯岡奈未, 禅正和真, 新居 麗, 園部奏生, 船越英丸, 中山恵利香, 進 浩太郎, 山本大地, Kyle Quin, 浅沼幹人

    第46回日本毒性学会学術年会  2019.6.26 

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    Event date: 2019.6.26 - 2019.6.28

    Language:Japanese   Presentation type:Poster presentation  

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  • Rotigotine protects dopaminergic neurons via astrocytic serotonin 1A receptors.

    Miyazaki, I, Isooka, N, Kikuoka, R, Wada, K, Nakayama, E, Shin, K, Yamamoto, D, Kitamura, Y, Asanuma, M

    第60回日本神経学会学術大会  2019.5.22 

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    Event date: 2019.5.22 - 2019.5.25

    Language:English   Presentation type:Poster presentation  

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  • 妊娠・授乳期にエポキシ樹脂曝露した新生仔マウスの脳発達に関する組織学的•行動学的解析.

    宮崎育子, 菊岡 亮, 磯岡奈未, 禅正和真, 新居 麗, 園部奏生, 船越英丸, 中山恵利香, 進 浩太郎, 山本大地, Kyle Quin, 浅沼幹人

    第124回日本解剖学会総会  2019.3.27 

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    Event date: 2019.3.27 - 2019.3.29

    Language:Japanese   Presentation type:Poster presentation  

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  • Treatment with coffee ingredients protects central and myenteric neurons in parkinsonian model.

    Miyazaki, I, Isooka, N, Wada, K, Kikuoka, R, Kitamura, Y, Asanuma, M

    第92回日本薬理学会年会  2019.3.14 

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    Event date: 2019.3.14 - 2019.3.16

    Language:English   Presentation type:Oral presentation (general)  

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  • 抗鬱薬ミルタザピンの神経ーグリア連関を介したドパミン神経保護効果.

    菊岡 亮, 宮崎育子, 久保田菜月, 前田恵実, 香川大樹, 守山雅晃, 粂 明日香, 村上真樹, 北村佳久, 浅沼幹人

    第134回日本薬理学会近畿部会 

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    Event date: 2018.11.23

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:神戸  

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  • ロテノン誘発神経毒性に対するカフェイン酸,クロロゲン酸の神経保護効果.

    磯岡奈未, 和田晃一, 古川智英子, 宮崎育子, 浅沼幹人

    第134回日本薬理学会近畿部会 

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    Event date: 2018.11.23

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:神戸  

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  • 実写3D解剖の開発と応用 エコーで見えないものが見えてくる解剖学.

    武田吉正, 假谷伸, 村井綾, 亀田雅博, 安原隆雄, 黒住和彦, 近藤喜太, 信岡大輔, 土井原博義, 笠原真悟, 浅沼幹人, 大塚愛二

    第80回日本臨床外科学会総会 

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    Event date: 2018.11.22

    Language:Japanese   Presentation type:Symposium, workshop panel (nominated)  

    Venue:東京  

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  • アストロサイトにおけるメタロチオネイン発現を標的とした神経保護.

    宮崎育子, 浅沼幹人

    日本毒性学会生体金属部会メタルバイオサイエンス研究会2018 

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    Event date: 2018.11.17

    Language:Japanese   Presentation type:Symposium, workshop panel (nominated)  

    Venue:仙台  

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  • パーキンソン病モデルマウスにおけるメタロチオネインを介したカフェイン酸,クロロゲン酸の神経保護効果.

    磯岡奈未, 和田晃一, 古川智英子, 宮崎育子, 浅沼幹人

    第45回日本毒性学会学術年会  メタルバイオサイエンス研究会2018

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    Event date: 2018.11.16

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:岡山  

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  • 抗うつ薬ミルタザピンによるアストロサイトの5-HT1A受容体を介したメタロチオネイン発現誘導とドパミン神経保護.

    菊岡 亮, 宮崎育子, 久保田菜月, 前田恵実, 香川大樹, 守山雅晃, 粂 明日香, 北村佳久, 浅沼幹人

    日本毒性学会生体金属部会メタルバイオサイエンス研究会2018 

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    Event date: 2018.11.16

    Language:Japanese   Presentation type:Poster presentation  

    Venue:仙台  

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  • 妊娠・授乳期エポキシ樹脂暴露産仔マウス脳への影響に関する組織学的・行動学的検討.

    浅沼幹人, 宮崎育子, 禅正和真, 菊岡 亮, 磯岡奈未, 新居 麗, 園部奏生, 船越英丸, 中山恵利香, 進 浩太郎, 山本大地, Kyle Quin

    日本解剖学会第73回中国・四国支部学術集会 

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    Event date: 2018.10.20 - 2018.10.21

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:岡山  

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  • アストロサイト: 抗てんかん薬のもうひとつの標的細胞. Invited

    浅沼幹人

    第12回香川小児てんかん懇話会 

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    Event date: 2018.10.19

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:高松  

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  • Neuroprotective effects of coffee ingredients against rotenone induced neurodegeneration in parkinsonian model. International conference

    Miyazaki, I., Isooka, N., Kikuoka, R., Wada, K., Kitamura, Y. and Asanuma, M.

    22nd International Congress of Parkinson’s Disease and Movement Disorders 

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    Event date: 2018.10.5 - 2018.10.9

    Language:English   Presentation type:Poster presentation  

    Venue:Hong Kong  

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  • Rotigotine protects dopaminergic neurons by targeting serotonin 1A receptors on astrocytes. International conference

    Asanuma, M., Miyazaki, I., Isooka, N., Kikuoka, R., Wada, K., Nakayama, E., Shin, K., Yamamoto, D., and Kitamura, Y.

    22nd International Congress of Parkinson’s Disease and Movement Disorders 

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    Event date: 2018.10.5 - 2018.10.9

    Language:English   Presentation type:Poster presentation  

    Venue:Hong Kong  

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  • アストロサイトの抗酸化防御機構を標的にした神経保護薬探索と末梢先行性のパーキンソン病病態におけるグリア細胞. Invited

    浅沼幹人

    第29回霧島神経薬理フォーラム 

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    Event date: 2018.8.18

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:由布市  

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  • 母体へのエポキシ樹脂BADGE暴露が新生仔マウス脳にもたらす影響.

    宮崎育子, 菊岡 亮, 磯岡奈未, 中山恵利香, 進 浩太郎, 山本大地, Quin E. Kyle, 船越英丸, 禅正和真, 浅沼幹人

    第45回日本毒性学会学術年会 

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    Event date: 2018.7.18 - 2018.7.20

    Language:Japanese   Presentation type:Poster presentation  

    Venue:岡山  

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  • メタンフェタミン神経毒性に対するHMGB1抗体の保護効果.

    黒田啓太, 磯岡奈未, 菊岡 亮, 村上真樹, 大熊 佑, 宮崎育子, 劉 克約, 西堀正洋, 浅沼幹人

    第29回創薬・薬理フォーラム岡山 

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    Event date: 2018.7.14

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:岡山  

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  • ロチゴチンによるアストロサイトのセロトニン1Aレセプターを標的としたドパミン神経保護.

    宮崎育子, 磯岡奈未, 菊岡 亮, 和田晃一, 中山恵利香, 進 浩太郎, 山本大地, 北村佳久, 浅沼幹人

    第12回パーキンソン病・運動障害疾患コングレス (MDSJ) 

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    Event date: 2018.7.5 - 2018.7.7

    Language:Japanese   Presentation type:Poster presentation  

    Venue:京都  

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  • Influence of benzodiazepine medications and GABAA receptor function on the pentobarbital-induced sleep behavior of lipopolysaccharide-treated mice. International conference

    Kitamura, Y., Okada, A., Hongo, S., Otsuki, K., Miki, A., Miyazaki, I., Asanuma, M. and Sendo, T.

    31st The International College of Neuropsychopharmacology (CINP World Congress) 

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    Event date: 2018.6.16 - 2018.6.19

    Language:English   Presentation type:Poster presentation  

    Venue:Vienna, Austria  

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  • Involvement of enhanced 5-HT2A receptor function on doxorubicin and cyclophosphamide-induced anxiety-like behavior in rats. International conference

    Naito, N., Kitamura, Y., Nakamura, Y., Sumiyoshi, Y., Kan, S., Miyazaki, I., Asanuma, M. and Sendo, T.

    31st The International College of Neuropsychopharmacology (CINP World Congress) 

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    Event date: 2018.6.16 - 2018.6.19

    Language:English   Presentation type:Poster presentation  

    Venue:Vienna, Austria  

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  • Possible involvement of metallothionein in rotenone-induced dopaminergic neurotoxicity.

    Miyazaki, I., Kikuoka, R., Isooka, N., Murakami, S., Kitamura, Y., Asanuma, M.

    第59回日本神経学会学術大会 

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    Event date: 2018.5.23 - 2018.5.26

    Language:English   Presentation type:Poster presentation  

    Venue:札幌  

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  • MeAV Anatomy: 最近のupdateと今後の展開.

    亀田雅博, 黒住和彦, 安原隆雄, 武田吉正, 浅沼幹人, 大塚愛二, 伊達 勲

    第32回日本微小脳神経外科解剖研究会 

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    Event date: 2018.4.21

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:高松  

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  • 妊娠・授乳期におけるエポキシ樹脂曝露の新生仔マウス脳への影響.

    宮崎育子, 菊岡 亮, 磯岡奈未, 船越英丸, Kyle Quin, 禅正和真, 村上真樹, 竹島美香, 三好 耕, 浅沼幹人

    第123回日本解剖学会総会 

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    Event date: 2018.3.28 - 2018.3.30

    Language:Japanese   Presentation type:Poster presentation  

    Venue:東京  

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  • アストロサイトの亜鉛関連分子を標的とした神経病態修飾薬. Disease-modifying drugs for neurodegenerative diseases targeting zinc-related molecules in astrocytes.

    浅沼幹人, 宮崎育子

    日本薬学会第138年会 

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    Event date: 2018.3.27

    Language:Japanese   Presentation type:Symposium, workshop panel (nominated)  

    Venue:金沢  

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  • アストロサイトを介した神経変性抑制. Invited

    浅沼幹人

    Current Trends in Parkinson's Disease 2018 

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    Event date: 2018.1.28

    Language:Japanese   Presentation type:Symposium, workshop panel (nominated)  

    Venue:東京  

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  • ロテノン誘発パーキンソン病モデルにおける腸管神経障害とコーヒー成分による神経保護効果.

    磯岡奈未, 和田晃一, 宮崎育子, 菊岡 亮, 古川智英子, 浅沼幹人

    第28回創薬・薬理フォーラム岡山  2017 

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    Event date: 2017.12.16

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:岡山  

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  • Mirtazapine exerts astrocyte-mediated dopaminergic neuroprotection. International conference

    Kikuoka, R., Miyazaki, I., Kubota, N., Maeda, M., Kagawa, D., Moriyama, M., Kume, A., Murakami, S., Kitamura, Y. and Asanuma, M.

    47th Annual Meeting of Society for Neuroscience (Neuroscience 2017)  2017 

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    Event date: 2017.11.11 - 2017.11.15

    Language:English   Presentation type:Poster presentation  

    Venue:Washington, DC  

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  • Effects of mirtazapine on doxorubicin and cyclophosphamide-induced spatial cognitive impairment and anxiety-like behavior in rats. International conference

    Nakamura, Y., Kitamura, Y., Naito, N., Sumiyoshi, Y., Miyazaki, I., Asanuma, M. and Sendo, T.

    47th Annual Meeting of Society for Neuroscience (Neuroscience 2017)  2017 

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    Event date: 2017.11.11 - 2017.11.15

    Language:English   Presentation type:Poster presentation  

    Venue:Washington, DC  

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  • Influence of nicotine on doxorubicin and cyclophosphamide-induced spatial cognitive impairment and anxiety-like behavior in rats. International conference

    Kitamura, Y., Sugimoto, M., Kanemoto, E., Machida, A., Nakamura, Y., Nanami, N., Miyazaki, I., Asanuma, M. and Sendo, T.

    47th Annual Meeting of Society for Neuroscience (Neuroscience 2017)  2017 

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    Event date: 2017.11.11 - 2017.11.15

    Language:English   Presentation type:Poster presentation  

    Venue:Washington, DC  

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  • 農薬ロテノン暴露による腸管神経障害とコーヒー成分による神経保護.

    宮崎育子, 磯岡奈未, 菊岡 亮, 和田晃一, 北村佳久, 浅沼幹人

    第11回パーキンソン病・運動障害疾患コングレス (MDSJ)  2017 

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    Event date: 2017.10.26 - 2017.10.28

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:品川  

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  • 農薬ロテノンによる非細胞自律性ドパミン神経障害へのメタロチオネインの関与.

    宮崎育子, 村上真樹, 菊岡 亮, 磯岡奈未, 北村佳久, 十川千春, 十川紀夫, 浅沼幹人

    日本毒性学会生体金属部会メタルバイオサイエンス研究会2017  2017 

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    Event date: 2017.10.13 - 2017.10.14

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:岡山  

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  • パーキンソン病モデルにおけるコーヒー成分の神経保護効果とメタロチオネイン発現誘導.

    磯岡奈未, 和田晃一, 宮崎育子, 古川智英子, 浅沼幹人

    日本毒性学会生体金属部会メタルバイオサイエンス研究会2017  2017 

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    Event date: 2017.10.13 - 2017.10.14

    Language:Japanese   Presentation type:Poster presentation  

    Venue:岡山  

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  • 抗うつ薬ミルタザピンによるアストロサイトのメタロチオネイン発現誘導がもたらすドパミン神経保護.

    菊岡 亮, 宮崎育子, 久保田菜月, 前田恵実, 香川大樹, 守山雅晃, 粂 明日香, 北村佳久, 浅沼幹人

    日本毒性学会生体金属部会メタルバイオサイエンス研究会2017  2017 

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    Event date: 2017.10.13 - 2017.10.14

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:岡山  

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  • 農薬ロテノンによるアストロサイト機能異常がもたらすドパミン神経障害.

    宮崎育子, 菊岡 亮, 磯岡奈未, 北村佳久, 浅沼幹人

    第39回日本生物学的精神医学会・第47回日本神経精神薬理学会合同年会  2017 

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    Event date: 2017.9.28 - 2017.9.30

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:札幌  

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  • コーヒー成分カフェイン酸,クロロゲン酸のPDモデルマウスにおける神経保護効果.

    磯岡奈未, 和田晃一, 宮崎育子, 浅沼幹人

    第39回日本生物学的精神医学会・第47回日本神経精神薬理学会合同年会  2017 

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    Event date: 2017.9.28 - 2017.9.30

    Language:Japanese   Presentation type:Poster presentation  

    Venue:札幌  

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  • アストロサイトを介したミルタザピンのドパミン神経保護に関する検討.

    菊岡 亮, 宮崎育子, 久保田菜月, 前田恵実, 香川大樹, 守山雅晃, 粂 明日香, 村上真樹, 北村佳久, 浅沼幹人

    第39回日本生物学的精神医学会・第47回日本神経精神薬理学会合同年会  2017 

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    Event date: 2017.9.28 - 2017.9.30

    Language:Japanese   Presentation type:Poster presentation  

    Venue:札幌  

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  • Rotenone-induced dopaminergic neurotoxicity promoted by mesencephalic astrocyte dysfunction. International conference

    Miyazaki, I., Murakami, S., Kikuoka, R., Isooka, N., Kitamura, Y. and Asanuma, M.

    23rd World Congress of Neurology  2017 

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    Event date: 2017.9.18

    Language:English   Presentation type:Poster presentation  

    Venue:Kyoto, Japan  

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  • Neuroprotective effects of rotigotine against dopaminergic neurodegeneration by targeting astrocytes. International conference

    Asanuma, M., Miyazaki, I., Isooka, N., Kikuoka, R., Wada, K., Nakayama, E., Shin, K., Yamamoto, D., and Kitamura, Y.

    23rd World Congress of Neurology  2017 

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    Event date: 2017.9.17

    Language:English   Presentation type:Poster presentation  

    Venue:Kyoto, Japan  

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  • ロテノン誘発パーキンソン病モデルへのコーヒー成分カフェイン酸,クロロゲン酸投与による神経保護効果.

    磯岡奈未, 和田晃一, 宮崎育子, 菊岡 亮, 浅沼幹人

    第27回創薬・薬理フォーラム岡山  2017 

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    Event date: 2017.7.29

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:岡山  

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  • 抗うつ薬ミルタザピンのアストロサイトにおけるメタロチオネイン発現誘導およびドパミン神経保護効果.

    菊岡 亮, 宮崎育子, 久保田菜月, 前田恵実, 香川大樹, 守山雅晃, 粂 明日香, 北村佳久, 浅沼幹人

    第27回創薬・薬理フォーラム岡山  2017 

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    Event date: 2017.7.29

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:岡山  

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  • 農薬ロテノンによる非細胞自律性ドパミン神経障害.

    宮崎育子, 村上真樹, 菊岡 亮, 磯岡奈未, 北村佳久, 浅沼幹人

    第44回日本毒性学会学術年会  2017 

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    Event date: 2017.7.10 - 2017.7.12

    Language:Japanese   Presentation type:Poster presentation  

    Venue:横浜  

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  • エポキシ樹脂BADGEの培養神経細胞への影響.

    浅沼幹人, 宮崎育子, 竹島美香, 中山恵利香, 進 浩太郎, Quin E. Kyle

    第44回日本毒性学会学術年会  2017 

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    Event date: 2017.7.10 - 2017.7.12

    Language:Japanese   Presentation type:Poster presentation  

    Venue:横浜  

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  • パーキンソン病での神経障害に対するコーヒー成分による腸内環境修飾の影響.

    浅沼幹人, 宮崎育子

    全日本コーヒー協会平成28年度研究成果報告会  2017 

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    Event date: 2017.6.16

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:岡山  

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  • Neuroprotective effects of antidepressant mirtazapine against dopaminergic neurodegeneration in cultured cells and in parkinsonian mice possibly by targeting astrocytes. International conference

    Asanuma, M., Miyazaki, I., Kikuoka, R., Murakami, S., Isooka, N. and Kitamura, Y.

    21st International Congress of Parkinson’s Disease and Movement Disorders  2017 

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    Event date: 2017.6.4 - 2017.6.8

    Language:English   Presentation type:Poster presentation  

    Venue:Vancouver, BC, Canada  

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  • Rotenone induces astrocyte-mediated non-cell autonomous dopaminergic neurotoxicity. International conference

    Miyazaki, I., Murakami, S., Kikuoka, R., Isooka, N., Kitamura, Y. and Asanuma, M.

    21st International Congress of Parkinson’s Disease and Movement Disorders  2017 

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    Event date: 2017.6.4 - 2017.6.8

    Language:English   Presentation type:Poster presentation  

    Venue:Vancouver, BC, Canada  

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  • 妊娠・授乳期におけるエポキシ樹脂暴露の産仔脳1次繊毛への影響.

    浅沼幹人, 宮崎育子, 竹島美香, 村上 真樹, 三好 耕

    第122回日本解剖学会総会・全国学術集会  2017 

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    Event date: 2017.3.30

    Language:Japanese   Presentation type:Poster presentation  

    Venue:長崎  

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  • セロトニン1Aアゴニストによる1次繊毛への影響.

    宮崎育子, 磯岡奈未, 粂 明日香, 三好 耕, 浅沼幹人

    第122回日本解剖学会総会・全国学術集会  2017 

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    Event date: 2017.3.28

    Language:Japanese   Presentation type:Poster presentation  

    Venue:長崎  

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  • 神経外環境からみたパーキンソン病の今

    浅沼幹人

    平成28年 第三内科同門会  2016 

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    Event date: 2016.12.11

    Language:Japanese   Presentation type:Oral presentation (invited, special)  

    Venue:岡山  

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  • 抗てんかん薬の作用点としてのアストロサイト

    浅沼幹人

    第50回日本てんかん学会学術集会  2016 

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    Event date: 2016.10.7

    Language:Japanese   Presentation type:Oral presentation (invited, special)  

    Venue:静岡  

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  • ALSモデルの運動障害および運動神経変性に対するセロトニン1Aアゴニストの抑制効果.

    浅沼幹人, 宮崎育子, 村上真樹, 鳥越奈央, 中野剛志, 菊岡 亮, 北村佳久, 千堂年昭

    第10回パーキンソン病・運動障害疾患コングレス  2016 

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    Event date: 2016.10.6 - 2016.10.8

    Language:Japanese   Presentation type:Poster presentation  

    Venue:京都  

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  • 農薬ロテノン暴露によるドパミン神経障害におけるアストロサイトの関与.

    宮崎育子, 村上真樹, 菊岡 亮, 磯岡奈未, 北村佳久, 浅沼幹人

    第10回パーキンソン病・運動障害疾患コングレス  2016 

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    Event date: 2016.10.6 - 2016.10.8

    Language:Japanese   Presentation type:Poster presentation  

    Venue:京都  

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  • パーキンソン病モデルマウスにおけるミルタザピンの神経保護効果.

    菊岡亮, 宮崎育子, 久保田菜月, 前田恵実, 香川大樹, 守山雅晃, 粂 明日香, 村上真樹, 北村佳久, 浅沼幹人, 千堂年昭

    第27回霧島神経薬理フォーラム  2016 

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    Event date: 2016.8.18

    Language:Japanese   Presentation type:Oral presentation (general)  

    Venue:志賀島  

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  • 抗うつ薬ミルタザピンのアストロサイトにおけるメタロチオネイン発現誘導およびドパミン神経保護効果.

    宮崎育子, 菊岡亮, 久保田菜月, 前田恵実, 香川大樹, 守山雅晃, 粂 明日香, 村上真樹, 北村佳久, 浅沼幹人

    メタルバイオサイエンス研究会サテライト2016  2016 

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    Event date: 2016.8.18

    Language:Japanese   Presentation type:Poster presentation  

    Venue:静岡  

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  • 筋萎縮性側索硬化症モデルにおける運動障害および運動神経変性に対する8-OH-DPATの抑制効果.

    浅沼幹人, 宮崎育子, 村上真樹, 鳥越奈央, 中野剛志, 菊岡 亮, 北村佳久, 千堂年昭

    第46回日本神経精神薬理学会年会  2016 

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    Event date: 2016.7.3

    Language:Japanese   Presentation type:Poster presentation  

    Venue:ソウル(韓国)  

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  • 抗うつ薬ミルタザピンのアストロサイトを標的としたドパミン神経保護.

    宮崎育子, 菊岡亮, 久保田菜月, 前田恵実, 香川大樹, 守山雅晃, 粂 明日香, 村上真樹, 北村佳久, 浅沼幹人

    第46回日本神経精神薬理学会年会  2016 

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    Event date: 2016.7.3

    Language:Japanese   Presentation type:Poster presentation  

    Venue:ソウル(韓国)  

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  • パーキンソン病モデルマウスにおけるミルタザピンの神経保護効果に関する検討.

    菊岡亮, 宮崎育子, 久保田菜月, 前田恵実, 香川大樹, 守山雅晃, 粂 明日香, 村上真樹, 北村佳久, 浅沼幹人

    第46回日本神経精神薬理学会年会  2016 

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    Event date: 2016.7.3

    Language:Japanese   Presentation type:Poster presentation  

    Venue:ソウル(韓国)  

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  • Mirtazapine protects dopaminergic neurons via astrocytes.

    Miyazaki, I., Kikuoka, R., Kubota, N., Maeda, M., Kagawa, D., Moriyama, M., Kume, A., Murakami, S., Kitamura, Y., Asanuma, M.

    第57回日本神経学会学術大会  2016 

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    Event date: 2016.5.21

    Language:English   Presentation type:Poster presentation  

    Venue:神戸  

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  • セロトニン1Aアゴニストによるアストロサイト1次繊毛の伸長.

    宮崎育子, 粂明日香, 三好耕, 浅沼幹人

    第121回日本解剖学会総会・全国学術集会  2016 

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    Event date: 2016.3.29

    Language:Japanese   Presentation type:Poster presentation  

    Venue:郡山  

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  • Rotenone-induced dopaminergic neurotoxicity mediated by astrocytes.

    Miyazaki, I., Murakami, S., Kikuoka, R., Isooka, N., Kitamura, Y. and Asanuma, M.

    第90回日本薬理学会年会  2016 

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    Event date: 2016.3.15

    Language:Japanese   Presentation type:Poster presentation  

    Venue:長崎  

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  • Neuroprotective effects of rotigotine in parkinsonian mice.

    Isooka, N., Miyazaki, I., Kikuoka, R., Wada, K., Nakayama, E., Yamamoto, D., Shin, K., Kitamura, Y. and Asanuma, M.

    第90回日本薬理学会年会  2016 

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    Event date: 2016.3.15

    Language:Japanese   Presentation type:Poster presentation  

    Venue:長崎  

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  • Serotonin 1A receptors on astrocytes as a target for dopaminergic neuroprotection.

    Miyazaki, I., Kikuoka, R., Kubota, N., Maeda, M., Kagawa, D., Moriyama, M., Kume, A., Murakami, S., Kitamura, Y., Asanuma, M.

    第89回日本薬理学会年会  2016 

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    Event date: 2016.3.11

    Language:Japanese   Presentation type:Poster presentation  

    Venue:横浜  

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  • Neuroprotective effect of fermented papaya preparation (SAIDO-PS501) via activation of astroglial anti-oxidative system.

    Murakami, S., Miyazaki, I., Asanuma, M.

    第89回日本薬理学会年会  2016 

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    Event date: 2016.3.10

    Language:Japanese   Presentation type:Poster presentation  

    Venue:横浜  

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  • アストロサイトを標的とした薬剤による神経変性疾患の病態修飾.

    浅沼幹人

    第24回創薬・薬理フォーラム岡山  2015 

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    Event date: 2015.12.20

    Language:Japanese   Presentation type:Oral presentation (invited, special)  

    Venue:岡山  

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  • Doxorubicin and cyclophosphamide treatment causes anxiety-like behavior and spatial cognition impairment in rats. International conference

    Kitamura, Y., Watanabe, S., Yoneda, S., Sugimoto, M., Kanemoto, E., Kanzaki, H., Machida, A., Miyazaki, I., Asanuma, M. and Sendo, T.

    45th Annual Meeting of Society for Neuroscience (Neuroscience 2015)  2015 

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    Event date: 2015.10.17 - 2015.10.21

    Language:English   Presentation type:Poster presentation  

    Venue:Chicago, IL  

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  • Effects of nicotine on doxorubicin and cyclophosphamide-induced spatial cognition and anxiety in rats International conference

    Sugimoto, M., Kanemoto, E., Watanabe, S., Miyazaki, I., Asanuma, M., Kitamura, Y. and Sendo, T.

    45th Annual Meeting of Society for Neuroscience (Neuroscience 2015)  2015 

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    Event date: 2015.10.17 - 2015.10.21

    Language:English   Presentation type:Poster presentation  

    Venue:Chicago, IL  

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  • パーキンソン病モデルマウスにおけるアストロサイトの5-HT1Aレセプターを標的とした神経保護.

    宮崎育子, 菊岡亮, 久保田菜月, 前田恵実, 香川大樹, 村上真樹, 北村佳久, 浅沼幹人

    第9回パーキンソン病・運動障害疾患コングレス  2015 

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    Event date: 2015.10.15 - 2015.10.17

    Language:Japanese   Presentation type:Poster presentation  

    Venue:東京  

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  • ミルタザピンのアストロサイトを標的としたドパミン神経保護効果.

    宮崎育子, 菊岡亮, 久保田菜月, 前田恵実, 香川大樹, 村上真樹, 北村佳久, 浅沼幹人

    第45回日本神経精神薬理学会 第37回日本生物学的精神医学会  2015 

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    Event date: 2015.9.24 - 2015.9.26

    Language:Japanese   Presentation type:Poster presentation  

    Venue:東京