Faculty Profiles - ASANUMA Masato

Papers - ASANUMA Masato

Division display 221 - 240 of about 318 ／ All the affair displays >>

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

Language：English Publishing type：Research paper (scientific journal) Publisher：P J D PUBLICATIONS LTD

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.

Web of Science

researchmap

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

Authorship：Lead author,　Corresponding author Language：English Publishing type：Research paper (scientific journal) Publisher：ARCH INT PHARMACODYNAMIE

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.

Web of Science

researchmap

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

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

Publishing type：Research paper (scientific journal) Publisher：SAGE Publications

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

Web of Science

researchmap

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

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

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

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

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

Language：English Publishing type：Research paper (scientific journal) Publisher：VSP BV

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.

Web of Science

researchmap

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

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

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

E. Iwata, M. Asanuma, Y. Kondo, S. Nishibayashi, K. Matsuura, N. Ogawa

Research Communications in Molecular Pathology and Pharmacology 88 ( 1 ) 31 - 38 1995

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

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.

Scopus

PubMed

researchmap

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

Language：English Publishing type：Research paper (scientific journal) Publisher：P J D PUBLICATIONS LTD

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 < 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<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.

Web of Science

researchmap

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

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

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

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

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

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

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

　 PREV - NEXT 　

< ASANUMA Masato >

Papers - ASANUMA Masato