2021/12/14 更新

写真a

ヨシダ リュウスケ
吉田 竜介
YOSHIDA Ryusuke
所属
医歯薬学域 教授
職名
教授
外部リンク

学位

  • 理学 ( 2002年3月   神戸大学大学院自然科学研究科 )

  • 博士(理学) ( 2002年3月   神戸大学 )

  • 修士(理学) ( 1998年3月   神戸大学 )

  • 学士(理学) ( 1996年3月   神戸大学 )

研究キーワード

  • 味覚

  • 食行動

  • 肥満

  • 神経科学

  • 健康科学

研究分野

  • ライフサイエンス / 常態系口腔科学  / 口腔生理学

学歴

  • 神戸大学   Graduate School of Science and Technology  

    1999年 - 2002年

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  • 神戸大学   Graduate School of Science and Technology  

    1996年 - 1998年

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  • 神戸大学   Faculty of Science   Department of Biology

    1992年 - 1996年

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経歴

  • 岡山大学   大学院医歯薬学総合研究院   教授

    2018年10月 - 現在

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  • 九州大学   OBT研究センター   准教授(兼任)

    2016年7月 - 2018年9月

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  • 九州大学   大学院歯学研究院   准教授

    2016年7月 - 2018年9月

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  • 九州大学   OBT研究センター   講師(兼任)

    2016年1月 - 2016年6月

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  • 九州大学   大学院歯学研究院   講師

    2012年4月 - 2016年6月

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  • 九州大学   大学院歯学研究院   助教

    2010年4月 - 2012年3月

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  • 九州大学   大学院歯学研究院   特任講師

    2009年6月 - 2010年3月

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  • 九州大学   大学院歯学研究院   助手(助教)

    2006年6月 - 2009年5月

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  • 九州大学   大学院歯学研究院   特任助手

    2005年12月 - 2006年5月

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  • 九州大学   大学院歯学研究院   学術研究員

    2003年4月 - 2005年11月

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  • 生物系特定産業技術研究推進機構   学術研究員

    2002年4月 - 2003年3月

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▼全件表示

所属学協会

 

論文

  • Phosphatidylinositol‐3 kinase mediates the sweet suppressive effect of leptin in mouse taste cells 査読

    Ryusuke Yoshida, Robert F. Margolskee, Yuzo Ninomiya

    Journal of Neurochemistry   2021年6月

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    担当区分:筆頭著者, 責任著者   記述言語:英語   掲載種別:研究論文(学術雑誌)  

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  • The sweet taste receptor, glucose transporters, and the ATP-sensitive K+ (KATP) channel: sugar sensing for the regulation of energy homeostasis 査読

    Ryusuke Yoshida, Keiko Yasumatsu, Yuzo Ninomiya

    Current Opinion in Physiology   20   57 - 63   2021年4月

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    担当区分:筆頭著者, 責任著者   記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:Elsevier BV  

    DOI: 10.1016/j.cophys.2021.01.009

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  • The sweet taste receptor, glucose transporters, andthe ATP-sensitive K+(KATP) channel: sugar sensingfor the regulation of energy homeostasis 招待 査読

    20   57 - 63   2021年1月

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    担当区分:筆頭著者, 責任著者   記述言語:英語   掲載種別:研究論文(学術雑誌)  

  • Orexin A and B in the rat superior salivatory nucleus 査読 国際誌

    Tadasu Sato, Takehiro Yajima, Masako Fujita, Motoi Kobashi, Hiroyuki Ichikawa, Ryusuke Yoshida, Yoshihiro Mitoh

    Autonomic Neuroscience   228   102712 - 102712   2020年11月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:Elsevier BV  

    Orexin (OX), which regulates sleep and wakefulness and feeding behaviors has 2 isoforms, orexin-A and -B (OXA and OXB). In this study, the distribution of OXA and OXB was examined in the rat superior salivatory nucleus (SSN) using retrograde tracing and immunohistochemical and methods. OXA- and OXB-immunoreactive (-ir) nerve fibers were seen throughout the SSN. These nerve fibers surrounded SSN neurons retrogradely labeled with Fast blue (FB) from the corda-lingual nerve. FB-positive neurons had pericellular OXA- (47.5%) and OXB-ir (49.0%) nerve fibers. Immunohistochemistry for OX receptors also demonstrated the presence of OX1R and OX2R in FB-positive SSN neurons. The majority of FB-positive SSN neurons contained OX1R- (69.7%) or OX2R-immunoreactivity (57.8%). These neurons had small and medium-sized cell bodies. In addition, half of FB-positive SSN neurons which were immunoreactive for OX1R (47.0%) and OX2R (52.2%) had pericellular OXA- and OXB-ir nerve fibers, respectively. Co-expression of OX1R- and OX2R was common in FB-positive SSN neurons. The present study suggests a possibility that OXs regulate the activity of SSN neurons through OX receptors.

    DOI: 10.1016/j.autneu.2020.102712

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  • Sodium‐glucose cotransporter 1 as a sugar taste sensor in mouse tongue 査読

    Keiko Yasumatsu, Tadahiro Ohkuri, Ryusuke Yoshida, Shusuke Iwata, Robert F. Margolskee, Yuzo Ninomiya

    Acta Physiologica   2020年7月

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    掲載種別:研究論文(学術雑誌)   出版者・発行元:Wiley  

    DOI: 10.1111/apha.13529

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    その他リンク: https://onlinelibrary.wiley.com/doi/full-xml/10.1111/apha.13529

  • The Effects of Mutual Interaction of Orexin-A and Glucagon-Like Peptide-1 on Reflex Swallowing Induced by SLN Afferents in Rats 査読

    Motoi Kobashi, Yuichi Shimatani, Masako Fujita, Yoshihiro Mitoh, Ryusuke Yoshida, Ryuji Matsuo

    International Journal of Molecular Sciences   21 ( 12 )   4422 - 4422   2020年6月

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    掲載種別:研究論文(学術雑誌)   出版者・発行元:MDPI AG  

    (1) Background: Our previous studies revealed that orexin-A, an appetite-increasing peptide, suppressed reflex swallowing via the commissural part of the nucleus tractus solitarius (cNTS), and that glucagon-like peptide-1 (GLP-1), an appetite-reducing peptide, also suppressed reflex swallowing via the medial nucleus of the NTS (mNTS). In this study, we examined the mutual interaction between orexin-A and GLP-1 in reflex swallowing. (2) Methods: Sprague–Dawley rats under urethane–chloralose anesthesia were used. Swallowing was induced by electrical stimulation of the superior laryngeal nerve (SLN) and was identified by the electromyographic (EMG) signals obtained from the mylohyoid muscle. (3) Results: The injection of GLP-1 (20 pmol) into the mNTS reduced the swallowing frequency and extended the latency of the first swallow. These suppressive effects of GLP-1 were not observed after the fourth ventricular administration of orexin-A. After the injection of an orexin-1 receptor antagonist (SB334867) into the cNTS, an ineffective dose of GLP-1 (6 pmol) into the mNTS suppressed reflex swallowing. Similarly, the suppressive effects of orexin-A (1 nmol) were not observed after the injection of GLP-1 (6 pmol) into the mNTS. After the administration of a GLP-1 receptor antagonist (exendin-4(5-39)), an ineffective dose of orexin-A (0.3 nmol) suppressed reflex swallowing. (4) Conclusions: The presence of reciprocal inhibitory connections between GLP-1 receptive neurons and orexin-A receptive neurons in the NTS was strongly suggested.

    DOI: 10.3390/ijms21124422

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  • Effects of bitter receptor antagonists on behavioral lick responses of mice 査読 国際誌

    Michimasa Masamoto, Yoshihiro Mitoh, Motoi Kobashi, Noriatsu Shigemura, Ryusuke Yoshida

    Neuroscience Letters   730   135041 - 135041   2020年6月

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    担当区分:責任著者   記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:Elsevier BV  

    Bitter taste receptors TAS2Rs detect noxious compounds in the oral cavity. Recent heterologous expression studies reported that some compounds function as antagonists for human TAS2Rs. For examples, amino acid derivatives such as γ-aminobutyric acid (GABA) and Nα,Nα-bis(carboxymethyl)-L-Lysine (BCML) blocked responses to quinine mediated by human TAS2R4. Probenecid inhibited responses to phenylthiocarbamide mediated by human TAS2R38. In this study, we investigated the effects of these human bitter receptor antagonists on behavioral lick responses of mice to elucidate whether these compounds also function as bitter taste blockers. In short-term (10 s) lick tests, concentration-dependent lick responses to bitter compounds (quinine-HCl, denatonium and phenylthiourea) were not affected by the addition of GABA or BCML. Probenecid reduced aversive lick responses to denatonium and phenylthiourea but not to quinine-HCl. In addition, taste cell responses to phenylthiourea were inhibited by probenecid. These results suggest some bitter antagonists of human TAS2Rs can work for bitter sense of mouse.

    DOI: 10.1016/j.neulet.2020.135041

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  • Expression of Renin-Angiotensin System Components in the Taste Organ of Mice. 査読 国際誌

    Noriatsu Shigemura, Shingo Takai, Fumie Hirose, Ryusuke Yoshida, Keisuke Sanematsu, Yuzo Ninomiya

    Nutrients   11 ( 9 )   E2251   2019年9月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    The systemic renin-angiotensin system (RAS) is an important regulator of body fluid and sodium homeostasis. Angiotensin II (AngII) is a key active product of the RAS. We previously revealed that circulating AngII suppresses amiloride-sensitive salt taste responses and enhances the responses to sweet compounds via the AngII type 1 receptor (AT1) expressed in taste cells. However, the molecular mechanisms underlying the modulation of taste function by AngII remain uncharacterized. Here we examined the expression of three RAS components, namely renin, angiotensinogen, and angiotensin-converting enzyme-1 (ACE1), in mouse taste tissues. We found that all three RAS components were present in the taste buds of fungiform and circumvallate papillae and co-expressed with αENaC (epithelial sodium channel α-subunit, a salt taste receptor) or T1R3 (taste receptor type 1 member 3, a sweet taste receptor component). Water-deprived mice exhibited significantly increased levels of renin expression in taste cells (p < 0.05). These results indicate the existence of a local RAS in the taste organ and suggest that taste function may be regulated by both locally-produced and circulating AngII. Such integrated modulation of peripheral taste sensitivity by AngII may play an important role in sodium/calorie homeostasis.

    DOI: 10.3390/nu11092251

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  • ヒト味覚認知閾値に対する低濃度塩添加の影響 査読

    吉田 竜介, 實松 敬介, 高井 信吾, 岩田 周介, 重村 憲徳

    日本味と匂学会誌   ( 第53回大会Proceeding集 )   S35 - S38   2019年9月

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    担当区分:筆頭著者, 責任著者   記述言語:日本語   出版者・発行元:日本味と匂学会  

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  • 摂食亢進ペプチドのラット顎下腺・舌下腺支配の副交感神経節前ニューロンに対する影響

    美藤 純弘, 佐藤 匡, 矢島 健大, 藤田 雅子, 小橋 基, 市川 博之, 吉田 竜介

    日本味と匂学会誌   ( 第53回大会Proceeding集 )   S55 - S58   2019年9月

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    記述言語:日本語   出版者・発行元:日本味と匂学会  

    視床下部に存在する10種類の摂食亢進ペプチドについて、ラット顎下腺・舌下腺支配の上唾液核(SSN)ニューロンを興奮させるかどうか検討した。Wistar系ラット(6〜14日齢)を用いて、標識ニューロンからホールセルパッチクランプ法により膜電位や膜電流を記録し、摂食亢進ペプチドをバス投与したときの影響を調べた。膜電位に対する応答では、orexin(OX)-Aに対する応答は他のペプチドと比較して有意に大きく、活動電位を伴うものがあった。また過分極応答を誘発するものはなかった。膜の入力抵抗に対する影響では、コントロールと比較してOX-A存在下では、同じ通電量60pAで発火頻度が増加した。また、通電ごとの平均の静止膜電位はコントロールでは-66mVであったのに対して、OX-A存在下では-59mVへと浅くなった。また、300nM OX-Aにより、多くのSSNニューロンが内向き電流を誘発していた。

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  • ヒト味覚認知閾値に対する低濃度塩添加の影響

    吉田 竜介, 實松 敬介, 高井 信吾, 岩田 周介, 重村 憲徳

    日本味と匂学会誌   ( 第53回大会Proceeding集 )   S35 - S38   2019年9月

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    記述言語:日本語   出版者・発行元:日本味と匂学会  

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  • Recognizing taste: coding patterns along the neural axis in mammals. 査読

    Chemical Senses   44   237 - 247   2019年5月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    DOI: 10.1093/chemse/bjz013

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  • Effects of insulin signaling on mouse taste cell proliferation. 査読 国際誌

    Shingo Takai, Yu Watanabe, Keisuke Sanematsu, Ryusuke Yoshida, Robert F Margolskee, Peihua Jiang, Ikiru Atsuta, Kiyoshi Koyano, Yuzo Ninomiya, Noriatsu Shigemura

    PloS one   14 ( 11 )   e0225190   2019年

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Expression of insulin and its receptor (IR) in rodent taste cells has been proposed, but exactly which types of taste cells express IR and the function of insulin signaling in taste organ have yet to be determined. In this study, we analyzed expression of IR mRNA and protein in mouse taste bud cells in vivo and explored its function ex vivo in organoids, using RT-PCR, immunohistochemistry, and quantitative PCR. In mouse taste tissue, IR was expressed broadly in taste buds, including in type II and III taste cells. With using 3-D taste bud organoids, we found insulin in the culture medium significantly decreased the number of taste cell and mRNA expression levels of many taste cell genes, including nucleoside triphosphate diphosphohydrolase-2 (NTPDase2), Tas1R3 (T1R3), gustducin, carbonic anhydrase 4 (CA4), glucose transporter-8 (GLUT8), and sodium-glucose cotransporter-1 (SGLT1) in a concentration-dependent manner. Rapamycin, an inhibitor of mechanistic target of rapamycin (mTOR) signaling, diminished insulin's effects and increase taste cell generation. Altogether, circulating insulin might be an important regulator of taste cell growth and/or proliferation via activation of the mTOR pathway.

    DOI: 10.1371/journal.pone.0225190

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  • Bitter Taste Responses of Gustducin-positive Taste Cells in Mouse Fungiform and Circumvallate Papillae. 査読 国際誌

    Ryusuke Yoshida, Shingo Takai, Keisuke Sanematsu, Robert F Margolskee, Noriatsu Shigemura, Yuzo Ninomiya

    Neuroscience   369   29 - 39   2018年1月

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    担当区分:筆頭著者, 責任著者   記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Bitter taste serves as an important signal for potentially poisonous compounds in foods to avoid their ingestion. Thousands of compounds are estimated to taste bitter and presumed to activate taste receptor cells expressing bitter taste receptors (Tas2rs) and coupled transduction components including gustducin, phospholipase Cβ2 (PLCβ2) and transient receptor potential channel M5 (TRPM5). Indeed, some gustducin-positive taste cells have been shown to respond to bitter compounds. However, there has been no systematic characterization of their response properties to multiple bitter compounds and the role of transduction molecules in these cells. In this study, we investigated bitter taste responses of gustducin-positive taste cells in situ in mouse fungiform (anterior tongue) and circumvallate (posterior tongue) papillae using transgenic mice expressing green fluorescent protein in gustducin-positive cells. The overall response profile of gustducin-positive taste cells to multiple bitter compounds (quinine, denatonium, cyclohexamide, caffeine, sucrose octaacetate, tetraethylammonium, phenylthiourea, L-phenylalanine, MgSO4, and high concentration of saccharin) was not significantly different between fungiform and circumvallate papillae. These bitter-sensitive taste cells were classified into several groups according to their responsiveness to multiple bitter compounds. Bitter responses of gustducin-positive taste cells were significantly suppressed by inhibitors of TRPM5 or PLCβ2. In contrast, several bitter inhibitors did not show any effect on bitter responses of taste cells. These results indicate that bitter-sensitive taste cells display heterogeneous responses and that TRPM5 and PLCβ2 are indispensable for eliciting bitter taste responses of gustducin-positive taste cells.

    DOI: 10.1016/j.neuroscience.2017.10.047

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  • The Role of Cholecystokinin in Peripheral Taste Signaling in Mice 査読

    Ryusuke Yoshida, Misa Shin, Keiko Yasumatsu, Shingo Takai, Mayuko Inoue, Noriatsu Shigemura, Soichi Takiguchi, Seiji Nakamura, Yuzo Ninomiya

    FRONTIERS IN PHYSIOLOGY   8   2017年10月

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    担当区分:筆頭著者   記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:FRONTIERS MEDIA SA  

    Cholecystokinin (CCK) is a gut hormone released from enteroendocrine cells. CCK functions as an anorexigenic factor by acting on CCK receptors expressed on the vagal afferent nerve and hypothalamus with a synergistic interaction between leptin. In the gut, tastants such as amino acids and bitter compounds stimulate CCK release from enteroendocrine cells via activation of taste transduction pathways. CCK is also expressed in taste buds, suggesting potential roles of CCK in taste signaling in the peripheral taste organ. In the present study, we focused on the function of CCK in the initial responses to taste stimulation. CCK was coexpressed with type II taste cellmarkers such as G alpha-gustducin, phospholipase C beta 2, and transient receptor potential channel M5. Furthermore, a small subset (similar to 30%) of CCK-expressing taste cells expressed a sweet/umami taste receptor component, taste receptor type 1 member 3, in taste buds. Because type II taste cells are sweet, umami or bitter taste cells, the majority of CCK-expressing taste cells may be bitter taste cells. CCK-A and -B receptors were expressed in both taste cells and gustatory neurons. CCK receptor knockout mice showed reduced neural responses to bitter compounds compared with wild-type mice. Consistently, intravenous injection of CCK-Ar antagonist lorglumide selectively suppressed gustatory nerve responses to bitter compounds. Intravenous injection of CCK-8 transiently increased gustatory nerve activities in a dose-dependent manner whereas administration of CCK-8 did not affect activities of bitter-sensitive taste cells. Collectively, CCK may be a functionally important neurotransmitter or neuromodulator to activate bitter nerve fibers in peripheral taste tissues.

    DOI: 10.3389/fphys.2017.00866

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  • LEPTIN SUPPRESSES SWEET TASTE RESPONSES OF ENTEROENDOCRINE STC-1 CELLS 査読

    Masafumi Jyotaki, Keisuke Sanematsu, Noriatsu Shigemura, Ryusuke Yoshida, Yuzo Ninomiya

    NEUROSCIENCE   332   76 - 87   2016年9月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:PERGAMON-ELSEVIER SCIENCE LTD  

    Leptin is an important hormone that regulates food intake and energy homeostasis by acting on central and peripheral targets. In the gustatory system, leptin is known to selectively suppress sweet responses by inhibiting the activation of sweet sensitive taste cells. Sweet taste receptor (T1R2 + T1R3) is also expressed in gut enteroendocrine cells and contributes to nutrient sensing, hormone release and glucose absorption. Because of the similarities in expression patterns between enteroendocrine and taste receptor cells, we hypothesized that they may also share similar mechanisms used to modify/regulate the sweet responsiveness of these cells by leptin. Here, we used mouse enteroendocrine cell line STC-1 and examined potential effect of leptin on Ca2+ responses of STC-1 cells to various taste compounds. Ca2+ responses to sweet compounds in STC-1 cells were suppressed by a rodent T1R3 inhibitor gurmarin, suggesting the involvement of T1R3-dependent receptors in detection of sweet compounds. Responses to sweet substances were suppressed by &gt;= 1 ng/ml leptin without affecting responses to bitter, umami and salty compounds. This effect was inhibited by a leptin antagonist (mutant L39A/D40A/F41A) and by ATP gated K+ (K-ATP) channel closer glibenclamide, suggesting that leptin affects sweet taste responses of enteroendocrine cells via activation of leptin receptor and KATP channel expressed in these cells. Moreover, leptin selectively inhibited sweet-induced but not bitter-induced glucagon-like peptide-1 (GLP-1) secretion from STC-1 cells. These results suggest that leptin modulates sweet taste responses of enteroendocrine cells to regulate nutrient sensing, hormone release and glucose absorption in the gut. (C) 2016 IBRO. Published by Elsevier Ltd. All rights reserved.

    DOI: 10.1016/j.neuroscience.2016.06.036

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  • Taste information derived from T1R-expressing taste cells in mice 査読

    Ryusuke Yoshida, Yuzo Ninomiya

    BIOCHEMICAL JOURNAL   473   525 - 536   2016年3月

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    担当区分:筆頭著者   記述言語:英語   出版者・発行元:PORTLAND PRESS LTD  

    The taste system of animals is used to detect valuable nutrients and harmful compounds in foods. In humans and mice, sweet, bitter, salty, sour and umami tastes are considered the five basic taste qualities. Sweet and umami tastes aremediated by G-protein-coupled receptors, belonging to the T1R (taste receptor type 1) family. This family consists of three members (T1R1, T1R2 and T1R3). They function as sweet or umami taste receptors by forming heterodimeric complexes, T1R1+T1R3 (umami) or T1R2+T1R3 (sweet). Receptors for each of the basic tastes are thought to be expressed exclusively in taste bud cells. Sweet (T1R2+T1R3-expressing) taste cells were thought to be segregated from umami (T1R1+T1R3-expressing) taste cells in taste buds. However, recent studies have revealed that a significant portion of taste cells in mice expressed all T1R subunits and responded to both sweet and umami compounds. This suggests that sweet and umami taste cells may not be segregated. Mice are able to discriminate between sweet and umami tastes, and both tastes contribute to behavioural preferences for sweet or umami compounds. There is growing evidence that T1R3 is also involved in behavioural avoidance of calcium tastes in mice, which implies that there may be a further population of T1R-expressing taste cells that mediate aversion to calcium taste. Therefore the simple view of detection and segregation of sweet and umami tastes by T1R-expressing taste cells, in mice, is now open to re-examination.

    DOI: 10.1042/BJ20151015

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  • Intracellular acidification is required for full activation of the sweet taste receptor by miraculin 査読

    Keisuke Sanematsu, Masayuki Kitagawa, Ryusuke Yoshida, Satoru Nirasawa, Noriatsu Shigemura, Yuzo Ninomiya

    SCIENTIFIC REPORTS   6   2016年3月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:NATURE PUBLISHING GROUP  

    Acidification of the glycoprotein, miraculin (MCL), induces sweet taste in humans, but not in mice. The sweet taste induced by MCL is more intense when acidification occurs with weak acids as opposed to strong acids. MCL interacts with the human sweet receptor subunit hTAS1R2, but the mechanisms by which the acidification of MCL activates the sweet taste receptor remain largely unexplored. The work reported here speaks directly to this activation by utilizing a sweet receptor TAS1R2 + TAS1R3 assay. In accordance with previous data, MCL-applied cells displayed a pH dependence with citric acid (weak acid) being right shifted to that with hydrochloric acid (strong acid). When histidine residues in both the intracellular and extracellular region of hTAS1R2 were exchanged for alanine, taste-modifying effect of MCL was reduced or abolished. Stronger intracellular acidification of HEK293 cells was induced by citric acid than by HCl and taste-modifying effect of MCL was proportional to intracellular pH regardless of types of acids. These results suggest that intracellular acidity is required for full activation of the sweet taste receptor by MCL.

    DOI: 10.1038/srep22807

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  • Peptide Signaling in Taste Transduction 査読

    Shingo Takai, Ryusuke Yoshida, Noriatsu Shigemura, Yuzo Ninomiya

    Chemosensory Transduction: The Detection of Odors, Tastes, and Other Chemostimuli   299 - 317   2016年2月

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    掲載種別:論文集(書籍)内論文  

    © 2016 Elsevier Inc. All rights reserved. Taste receptor cells sense various chemical compounds in foods and transmit these signals through gustatory nerve fibers to the central nervous system. These sensory signals are vitally important for life; they provide information about which prospective foods are nutritious and warnings as to those that are noxious. Recent studies have revealed the involvement of multifarious bioactive peptides, many of which are primarily identified organs such as the gastrointestinal tract, in the modulation of taste responses. These peptides affect peripheral taste responsiveness of animals and play important roles in the regulation of feeding behavior and the maintenance of homeostasis. In this chapter, we discuss the various functions of peptide signaling in the peripheral taste system.

    DOI: 10.1016/B978-0-12-801694-7.00017-2

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  • The function of glucagon-like peptide-1 in the mouse peripheral taste system 査読

    Takai Shingo, Yoshida Ryusuke, Yasumatsu Keiko, Shigemura Noriatsu, Ninomiya Yuzo

    JOURNAL OF ORAL BIOSCIENCES   58 ( 1 )   10 - 15   2016年2月

  • Leptin Suppresses Mouse Taste Cell Responses to Sweet Compounds 査読

    Ryusuke Yoshida, Kenshi Noguchi, Noriatsu Shigemura, Masafumi Jyotaki, Ichiro Takahashi, Robert F. Margolskee, Yuzo Ninomiya

    DIABETES   64 ( 11 )   3751 - 3762   2015年11月

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    担当区分:筆頭著者   記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER DIABETES ASSOC  

    Leptin is known to selectively suppress neural and behavioral responses to sweet-tasting compounds. However, the molecular basis for the effect of leptin on sweet taste is not known. Here, we report that leptin suppresses sweet taste via leptin receptors (Ob-Rb) and K-ATP channels expressed selectively in sweet-sensitive taste cells. Ob-Rb was more often expressed in taste cells that expressed T1R3 (a sweet receptor component) than in those that expressed glutamate-aspartate transporter (a marker for Type I taste cells) or GAD67 (a marker for Type III taste cells). Systemically administered leptin suppressed taste cell responses to sweet but not to bitter or sour compounds. This effect was blocked by a leptin antagonist and was absent in leptin receptor deficient db/db mice and mice with diet-induced obesity. Blocking the K-ATP channel subunit sulfonylurea receptor 1, which was frequently coexpressed with Ob-Rb in T1R3-expressing taste cells, eliminated the effect of leptin on sweet taste. In contrast, activating the K-ATP channel with diazoxide mimicked the sweet-suppressing effect of leptin. These results indicate that leptin acts via Ob-Rb and K-ATP channels that are present in T1R3-expressing taste cells to selectively suppress their responses to sweet compounds.

    DOI: 10.2337/db14-1462

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  • Glucagon-like peptide-1 is specifically involved in sweet taste transmission 査読

    Shingo Takai, Keiko Yasumatsu, Mayuko Inoue, Shusuke Iwata, Ryusuke Yoshida, Noriatsu Shigemura, Yuchio Yanagawa, Daniel J. Drucker, Robert F. Margolskee, Yuzo Ninomiya

    FASEB JOURNAL   29 ( 6 )   2268 - 2280   2015年6月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:FEDERATION AMER SOC EXP BIOL  

    Five fundamental taste qualities (sweet, bitter, salty, sour, umami) are sensed by dedicated taste cells (TCs) that relay quality information to gustatory nerve fibers. In peripheral taste signaling pathways, ATP has been identified as a functional neurotransmitter, but it remains to be determined how specificity of different taste qualities is maintained across synapses. Recent studies demonstrated that some gut peptides are released from taste buds by prolonged application of particular taste stimuli, suggesting their potential involvement in taste information coding. In this study, we focused on the function of glucagon-like peptide-1 (GLP-1) in initial responses to taste stimulation. GLP-1 receptor (GLP-1R) null mice had reduced neural and behavioral responses specifically to sweet compounds compared to wild-type (WT) mice. Some sweet responsive TCs expressed GLP-1 and its receptors were expressed in gustatory neurons. GLP-1 was released immediately from taste bud cells in response to sweet compounds but not to other taste stimuli. Intravenous administration of GLP-1 elicited transient responses in a subset of sweet-sensitive gustatory nerve fibers but did not affect other types of fibers, and this response was suppressed by pre-administration of the GLP-1R antagonist Exendin-4(3-39). Thus GLP-1 may be involved in normal sweet taste signal transmission in mice.

    DOI: 10.1096/fj.14-265355

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  • Modulation of sweet taste sensitivities by endogenous leptin and endocannabinoids in mice 査読

    Mayu Niki, Masafumi Jyotaki, Ryusuke Yoshida, Keiko Yasumatsu, Noriatsu Shigemura, Nicholas V. DiPatrizio, Daniele Piomelli, Yuzo Ninomiya

    JOURNAL OF PHYSIOLOGY-LONDON   593 ( 11 )   2527 - 2545   2015年6月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:WILEY-BLACKWELL  

    Potential roles of endogenous leptin and endocannabinoids in sweet taste were examined by using pharmacological antagonists and mouse models including leptin receptor deficient (db/db) and diet-induced obese (DIO) mice. Chorda tympani (CT) nerve responses of lean mice to sweet compounds were increased after administration of leptin antagonist (LA) but not affected by administration of cannabinoid receptor antagonist (AM251).db/db mice showed clear suppression of CT responses to sweet compounds after AM251, increased endocannabinoid levels in the taste organ, and enhanced expression of a biosynthesizing enzyme of endocannabinoids in taste cells. The effect of LA was gradually decreased and that of AM251 was increased during the course of obesity in DIO mice. These findings suggest that circulating leptin, but not local endocannabinoids, is a dominant modulator for sweet taste in lean mice and endocannabinoids become more effective modulators of sweet taste under conditions of deficient leptin signalling.
    AbstractLeptin is an anorexigenic mediator that reduces food intake by acting on hypothalamic receptor Ob-Rb. In contrast, endocannabinoids are orexigenic mediators that act via cannabinoid CB1 receptors in hypothalamus, limbic forebrain, and brainstem. In the peripheral taste system, leptin administration selectively inhibits behavioural, taste nerve and taste cell responses to sweet compounds. Opposing the action of leptin, endocannabinoids enhance sweet taste responses. However, potential roles of endogenous leptin and endocannabinoids in sweet taste remain unclear. Here, we used pharmacological antagonists (Ob-Rb: L39A/D40A/F41A (LA), CB1: AM251) and examined the effects of their blocking activation of endogenous leptin and endocannabinoid signalling on taste responses in lean control, leptin receptor deficient db/db, and diet-induced obese (DIO) mice. Lean mice exhibited significant increases in chorda tympani (CT) nerve responses to sweet compounds after LA administration, while they showed no significant changes in CT responses after AM251. In contrast, db/db mice showed clear suppression of CT responses to sweet compounds after AM251, increased endocannabinoid (2-arachidonoyl-sn-glycerol (2-AG)) levels in the taste organ, and enhanced expression of a biosynthesizing enzyme (diacylglycerol lipase (DAGL)) of 2-AG in taste cells. In DIO mice, the LA effect was gradually decreased and the AM251 effect was increased during the course of obesity. Taken together, our results suggest that circulating leptin, but not local endocannabinoids, may be a dominant modulator for sweet taste in lean mice; however, endocannabinoids may become more effective modulators of sweet taste under conditions of deficient leptin signalling, possibly due to increased production of endocannabinoids in taste tissue.

    DOI: 10.1113/JP270295

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  • Involvement of multiple taste receptors in umami taste: analysis of gustatory nerve responses in metabotropic glutamate receptor 4 knockout mice 査読

    Keiko Yasumatsu, Tomohiro Manabe, Ryusuke Yoshida, Ken Iwatsuki, Hisayuki Uneyama, Ichiro Takahashi, Yuzo Ninomiya

    JOURNAL OF PHYSIOLOGY-LONDON   593 ( 4 )   1021 - 1034   2015年2月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:WILEY  

    The taste receptor T1R1+T1R3 heterodimer and metabotropic glutamate receptors (mGluR) may function as umami taste receptors. Here, we used mGluR4 knockout (mGluR4-KO) mice and examined the function of mGluR4 in peripheral taste responses of mice. The mGluR4-KO mice showed reduced responses to glutamate and l-AP4 (mGluR4 agonist) in the chorda tympani and glossopharyngeal nerves without affecting responses to other taste stimuli. Residual glutamate responses in mGluR4-KO mice were suppressed by gurmarin (T1R3 blocker) and AIDA (group I mGluR antagonist). The present study not only provided functional evidence for the involvement of mGluR4 in umami taste responses, but also suggested contributions of T1R1+T1R3 and mGluR1 receptors in glutamate responses.
    AbstractUmami taste is elicited by l-glutamate and some other amino acids and is thought to be initiated by G-protein-coupled receptors. Proposed umami receptors include heterodimers of taste receptor type 1, members 1 and 3 (T1R1+T1R3), and metabotropic glutamate receptors 1 and 4 (mGluR1 and mGluR4). Accumulated evidences support the involvement of T1R1+T1R3 in umami responses in mice. However, little is known about the in vivo function of mGluR in umami taste. Here, we examined taste responses of the chorda tympani (CT) and the glossopharyngeal (GL) nerves in wild-type mice and mice genetically lacking mGluR4 (mGluR4-KO). Our results indicated that compared to wild-type mice, mGluR4-KO mice showed significantly smaller gustatory nerve responses to glutamate and l-(+)-2-amino-4-phosphonobutyrate (an agonist for group III mGluR) in both the CT and GL nerves without affecting responses to other taste stimuli. Residual glutamate responses in mGluR4-KO mice were not affected by (RS)-alpha-cyclopropyl-4-phosphonophenylglycine (an antagonist for group III mGluR), but were suppressed by gurmarin (a T1R3 blocker) in the CT and (RS)-1-aminoindan-1,5-dicarboxylic acid (an antagonist for group I mGluR) in the CT and GL nerve. In wild-type mice, both quisqualic acid (an agonist for group I mGluR) and l-(+)-2-amino-4-phosphonobutyrate elicited gustatory nerve responses and these responses were suppressed by addition of (RS)-1-aminoindan-1,5-dicarboxylic acid and (RS)-alpha-cyclopropyl-4-phosphonophenylglycine, respectively. Collectively, the present study provided functional evidences for the involvement of mGluR4 in umami taste responses in mice. The results also suggest that T1R1+T1R3 and mGluR1 are involved in umami taste responses in mice. Thus, umami taste would be mediated by multiple receptors.

    DOI: 10.1113/jphysiol.2014.284703

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  • アンギオテンシンIIによるエンドカンナビノイド受容体を介した甘味の増強

    岩田 周介, 吉田 竜介, 重村 憲徳, 二ノ宮 裕三

    日本味と匂学会誌   21 ( 3 )   259 - 262   2014年12月

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    記述言語:日本語   出版者・発行元:日本味と匂学会  

    アンジオテンシンII(Ang II)は血圧や体内Na+濃度を調節するホルモンであるが、近年著者らはAng IIが末梢の味覚器にもAng II type I受容体(AT1)を介して作用し、塩味感受性を修飾するのみならず、甘味感受性を増強することを発見した。この甘味増強作用は、摂食促進因子エンドカンナビノイド(eCB)の受容体(CB1)欠損マウスではみられなかったことから、Ang IIを介した甘味増強作用にはeCB系が関与する可能性が示唆されたが、その詳細はほとんど不明であった。今回、この点を明らかにするため、マウスを用いて様々な実験を行った。その結果、Ang IIによる甘味感受性の増強は、AT1シグナル下流で産生されるDiacylglycerolがDiacylglycerol lipaseの作用によって2-Arachidonoylglycerolに変換され、これが甘味細胞に発現するCB1を活性化することで生じる可能性が示唆された。

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    その他リンク: https://search.jamas.or.jp/index.php?module=Default&action=Link&pub_year=2014&ichushi_jid=J04102&link_issn=&doc_id=20150212090011&doc_link_id=%2Fcw7jasts%2F2014%2F002103%2F014%2F0259-0262%26dl%3D0&url=http%3A%2F%2Fwww.medicalonline.jp%2Fjamas.php%3FGoodsID%3D%2Fcw7jasts%2F2014%2F002103%2F014%2F0259-0262%26dl%3D0&type=MedicalOnline&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00004_2.gif

  • 若手の口腔生理学研究最前線 味蕾から分泌される消化管ホルモンは味質特異的な情報伝達に関与する

    高井 信吾, 安松 啓子, 岩田 周介, 井上 真由子, 吉田 竜介, 重村 憲徳, Drucker Daniel J., Margolskee Robert F., 二ノ宮 裕三

    Journal of Oral Biosciences Supplement   2014   89 - 89   2014年9月

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    記述言語:日本語   出版者・発行元:(一社)歯科基礎医学会  

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  • Taste Transductions in Taste Receptor Cells: Basic Tastes and Moreover 査読

    Shusuke Iwata, Ryusuke Yoshida, Yuzo Ninomiya

    CURRENT PHARMACEUTICAL DESIGN   20 ( 16 )   2684 - 2692   2014年5月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:BENTHAM SCIENCE PUBL LTD  

    In the oral cavity, taste receptor cells dedicate to detecting chemical compounds in foodstuffs and transmitting their signals to gustatory nerve fibers. Heretofore, five taste qualities (sweet, umami, bitter, salty and sour) are generally accepted as basic tastes. Each of these may have a specific role in the detection of nutritious and poisonous substances; sweet for carbohydrate sources of calories, umami for protein and amino acid contents, bitter for harmful compounds, salty for minerals and sour for ripeness of fruits and spoiled foods. Recent studies have revealed molecular mechanisms for reception and transduction of these five basic tastes. Sweet, umami and bitter tastes are mediated by G-protein coupled receptors (GPCRs) and second-messenger signaling cascades. Salty and sour tastes are mediated by channel-type receptors. In addition to five basic tastes, taste receptor cells may have the ability to detect fat taste, which is elicited by fatty acids, and calcium taste, which is elicited by calcium. Taste compounds eliciting either fat taste or calcium taste may be detected by specific GPCRs expressed in taste receptor cells. This review will focus on transduction mechanisms and cellular characteristics responsible for each of basic tastes, fat taste and calcium taste.

    DOI: 10.2174/13816128113199990575

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  • Structure, Function, and Signaling of Taste G-Protein-Coupled Receptors 査読

    Keisuke Sanematsu, Ryusuke Yoshida, Noriatsu Shigemura, Yuzo Ninomiya

    CURRENT PHARMACEUTICAL BIOTECHNOLOGY   15 ( 10 )   951 - 961   2014年

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:BENTHAM SCIENCE PUBL LTD  

    Detection of tastes is critical for animals. Sweet, umami and bitter taste are mediated by G-protein-coupled receptors that are expressed in the taste receptor cells. TAS1Rs which belong to class C G-protein-coupled receptors form heterodimeric complexes to function as sweet (TAS1R2 + TAS1R3) or umami (TAS1R1 + TAS1R3) taste receptors. Umami taste is also considered to be mediated by mGluRs. TAS2Rs belong to class A G-protein-coupled receptors and are responsible for bitter taste. After activation of these receptors, their second messenger pathways lead to depolarization and intracellular calcium increase in taste receptor cells. Then, transmitter is released from taste receptor cells leading to activation of taste nerve fibers and taste information is sent to the central nervous system. Recent studies on heterologous expression system and molecular modeling lead to better understanding of binding site of TAS1Rs and TAS2Rs and molecular mechanisms for interaction between taste substances and these receptors. TAS1Rs and TAS2Rs have multiple and single binding sites for structurally diverse ligands, respectively. Sensitivities of these receptors are known to differ among individuals, strains, and species. In addition, some species abolish these receptors and signaling molecules. Here we focus on structure, function, signaling, polymorphism, and molecular evolution of the taste G-protein-coupled receptors.

    DOI: 10.2174/1389201015666140922105911

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  • 味神経に発現するGLP-1レセプターとその役割 査読

    髙井 信吾, 安松 啓子, 吉田 竜介, 重村 憲徳, 二ノ宮 裕三

    日本味と匂学会 学会誌   21   2014年

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    記述言語:日本語   掲載種別:研究論文(学術雑誌)  

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  • Angiotensin II Modulates Salty and Sweet Taste Sensitivities 査読

    Noriatsu Shigemura, Shusuke Iwata, Keiko Yasumatsu, Tadahiro Ohkuri, Nao Horio, Keisuke Sanematsu, Ryusuke Yoshida, Robert F. Margolskee, Yuzo Ninomiya

    JOURNAL OF NEUROSCIENCE   33 ( 15 )   6267 - 6277   2013年4月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:SOC NEUROSCIENCE  

    Understanding the mechanisms underlying gustatory detection of dietary sodium is important for the prevention and treatment of hypertension. Here, we show that Angiotensin II (AngII), a major mediator of body fluid and sodium homeostasis, modulates salty and sweet taste sensitivities, and that this modulation critically influences ingestive behaviors in mice. Gustatory nerve recording demonstrated that AngII suppressed amiloride-sensitive taste responses to NaCl. Surprisingly, AngII also enhanced nerve responses to sweeteners, but had no effect on responses to KCl, sour, bitter, or umamitastants. These effects of AngII on nerve responses were blocked by the angiotensin II type 1 receptor (AT1) antagonist CV11974. In behavioral tests, CV11974 treatment reduced the stimulated high licking rate to NaCl and sweeteners in water-restricted mice with elevated plasma AngII levels. In taste cells AT1 proteins were coexpressed with alpha ENaC (epithelial sodium channel alpha-subunit, an amiloride-sensitive salt taste receptor) or T1r3 (a sweet taste receptor component). These results suggest that the taste organ is a peripheral target of AngII. The specific reduction of amiloride-sensitive salt taste sensitivity by AngII may contribute to increased sodium intake. Furthermore, AngII may contribute to increased energy intake by enhancing sweet responses. The linkage between salty and sweet preferences via AngII signaling may optimize sodium and calorie intakes.

    DOI: 10.1523/JNEUROSCI.5599-12.2013

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  • Taste responses in mice lacking taste receptor subunit T1R1 査読

    Yoko Kusuhara, Ryusuke Yoshida, Tadahiro Ohkuri, Keiko Yasumatsu, Anja Voigt, Sandra Huebner, Katsumasa Maeda, Ulrich Boehm, Wolfgang Meyerhof, Yuzo Ninomiya

    JOURNAL OF PHYSIOLOGY-LONDON   591 ( 7 )   1967 - 1985   2013年4月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:WILEY-BLACKWELL  

    The T1R1 receptor subunit acts as an umami taste receptor in combination with its partner, T1R3. In addition, metabotropic glutamate receptors (brain and taste variants of mGluR1 and mGluR4) are thought to function as umami taste receptors. To elucidate the function of T1R1 and the contribution of mGluRs to umami taste detection in vivo, we used newly developed knock-out (T1R1/) mice, which lack the entire coding region of the Tas1r1 gene and express mCherry in T1R1-expressing cells. Gustatory nerve recordings demonstrated that T1R1/ mice exhibited a serious deficit in inosine monophosphate-elicited synergy but substantial residual responses to glutamate alone in both chorda tympani and glossopharyngeal nerves. Interestingly, chorda tympani nerve responses to sweeteners were smaller in T1R1/ mice. Taste cell recordings demonstrated that many mCherry-expressing taste cells in T1R1+/ mice responded to sweet and umami compounds, whereas those in T1R1/ mice responded to sweet stimuli. The proportion of sweet-responsive cells was smaller in T1R1/ than in T1R1+/ mice. Single-cell RT-PCR demonstrated that some single mCherry-expressing cells expressed all three T1R subunits. Chorda tympani and glossopharyngeal nerve responses to glutamate were significantly inhibited by addition of mGluR antagonists in both T1R1/ and T1R1+/ mice. Conditioned taste aversion tests demonstrated that both T1R1/ and T1R1+/ mice were equally capable of discriminating glutamate from other basic taste stimuli. Avoidance conditioned to glutamate was significantly reduced by addition of mGluR antagonists. These results suggest that T1R1-expressing cells mainly contribute to umami taste synergism and partly to sweet sensitivity and that mGluRs are involved in the detection of umami compounds.

    DOI: 10.1113/jphysiol.2012.236604

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  • Modulation of sweet responses of taste receptor cells 査読

    Ryusuke Yoshida, Mayu Niki, Masafumi Jyotaki, Keisuke Sanematsu, Noriatsu Shigemura, Yuzo Ninomiya

    SEMINARS IN CELL & DEVELOPMENTAL BIOLOGY   24 ( 3 )   226 - 231   2013年3月

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    記述言語:英語   出版者・発行元:ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD  

    Taste receptor cells play a major role in detection of chemical compounds in the oral cavity. Information derived from taste receptor cells, such as sweet, bitter, salty, sour and umami is important for evaluating the quality of food components. Among five basic taste qualities, sweet taste is very attractive for animals and influences food intake. Recent studies have demonstrated that sweet taste sensitivity in taste receptor cells would be affected by leptin and endocannabinoids. Leptin is an anorexigenic mediator that reduces food intake by acting on leptin receptor Ob-Rb in the hypothalamus. Endocannabinoids such as anandamide [N-arachidonoylethanolamine (AEA)] and 2-arachidonoyl glycerol (2-AG) are known as orexigenic mediators that act via cannabinoid receptor 1 (CB1) in the hypothalamus and limbic forebrain to induce appetite and stimulate food intake. At the peripheral gustatory organs, leptin selectively suppresses and endocannabinoids selectively enhance sweet taste sensitivity via Ob-Rb and CB1 expressed in sweet sensitive taste cells. Thus leptin and endocannabinoids not only regulate food intake via central nervous systems but also modulate palatability of foods by altering peripheral sweet taste responses. Such reciprocal modulation of leptin and endocannabinoids on peripheral sweet sensitivity may play an important role in regulating energy homeostasis. (C) 2012 Elsevier Ltd. All rights reserved.

    DOI: 10.1016/j.semcdb.2012.08.004

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  • Umami taste in mice uses multiple receptors and transduction pathways 査読

    Keiko Yasumatsu, Yoko Ogiwara, Shingo Takai, Ryusuke Yoshida, Ken Iwatsuki, Kunio Torii, Robert F. Margolskee, Yuzo Ninomiya

    JOURNAL OF PHYSIOLOGY-LONDON   590 ( 5 )   1155 - 1170   2012年2月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:WILEY  

    The distinctive umami taste elicited by L-glutamate and some other amino acids is thought to be initiated by G-protein-coupled receptors. Proposed umami receptors include heteromers of taste receptor type 1, members 1 and 3 (T1R1+ T1R3), andmetabotropic glutamate receptors 1 and 4 (mGluR1 and mGluR4). Multiple lines of evidence support the involvement of T1R1+ T1R3 in umami responses of mice. Although several studies suggest the involvement of receptors other than T1R1+ T1R3 in umami, the identity of those receptors remains unclear. Here, we examined taste responsiveness of umami-sensitive chorda tympani nerve fibres fromwild-type mice andmice genetically lacking T1R3 or its downstream transduction molecule, the ion channel TRPM5. Our results indicate that single umami-sensitive fibres in wild-type mice fall into two major groups: sucrose-best (S-type) andmonopotassium glutamate (MPG)-best (M-type). Each fibre type has two subtypes; one shows synergism between MPG and inosine monophosphate (S1, M1) and the other shows no synergism (S2, M2). In both T1R3 and TRPM5 null mice, S1-type fibres were absent, whereas S2-, M1-and M2-types remained. Lingual application of mGluR antagonists selectively suppressedMPG responses of M1-andM2-type fibres. These data suggest the existence of multiple receptors and transduction pathways for umami responses in mice. Information initiated from T1R3-containing receptors may be mediated by a transduction pathway including TRPM5 and conveyed by sweet-best fibres, whereas umami information from mGluRs may be mediated by TRPM5-independent pathway(s) and conveyed by glutamate-best fibres.

    DOI: 10.1113/jphysiol.2011.211920

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  • Responses to Apical and Basolateral Application of Glutamate in Mouse Fungiform Taste Cells with Action Potentials 査読

    Mayu Niki, Shingo Takai, Yoko Kusuhara, Yuzo Ninomiya, Ryusuke Yoshida

    CELLULAR AND MOLECULAR NEUROBIOLOGY   31 ( 7 )   1033 - 1040   2011年10月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:SPRINGER/PLENUM PUBLISHERS  

    In taste bud cells, glutamate may elicit two types of responses, as an umami tastant and as a neurotransmitter. Glutamate applied to apical membrane of taste cells would elicit taste responses whereas glutamate applied to basolateral membrane may act as a neurotransmitter. Using restricted stimulation to apical or basolateral membrane of taste cells, we examined responses of taste cells to glutamate stimulation, separately. Apical application of monosodium glutamate (MSG, 0.3 M) increased firing frequency in some of mouse fungiform taste cells that evoked action potentials. These cells were tested with other basic taste compounds, NaCl (salty), saccharin (sweet), HCl (sour), and quinine (bitter). MSG-sensitive taste cells could be classified into sweet-best (S-type), MSG-best (M-type), and NaCl or other electrolytes-best (N- or E/H-type) cells. Furthermore, S- and M-type could be classified into two sub-types according to the synergistic effect between MSG and inosine-5&apos;-monophosphate (S1, M1 with synergism; S2, M2 without synergism). Basolateral application of glutamate (100 mu M) had almost no effect on the mean spontaneous firing rates in taste cells. However, about 10% of taste cells tested showed transient increases in spontaneous firing rates (&gt; mean + 2 standard deviation) after basolateral application of glutamate. These results suggest the existence of multiple types of umami-sensitive taste cells and the existence of glutamate receptor(s) on the basolateral membrane of a subset of taste cells.

    DOI: 10.1007/s10571-011-9702-5

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  • Sour Taste Responses in Mice Lacking PKD Channels 査読

    Nao Horio, Ryusuke Yoshida, Keiko Yasumatsu, Yuchio Yanagawa, Yoshiro Ishimaru, Hiroaki Matsunami, Yuzo Ninomiya

    PLOS ONE   6 ( 5 )   2011年5月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:PUBLIC LIBRARY SCIENCE  

    Background: The polycystic kidney disease-like ion channel PKD2L1 and its associated partner PKD1L3 are potential candidates for sour taste receptors. PKD2L1 is expressed in type III taste cells that respond to sour stimuli and genetic elimination of cells expressing PKD2L1 substantially reduces chorda tympani nerve responses to sour taste stimuli. However, the contribution of PKD2L1 and PKD1L3 to sour taste responses remains unclear.
    Methodology/Principal Findings: We made mice lacking PKD2L1 and/or PKD1L3 gene and investigated whole nerve responses to taste stimuli in the chorda tympani or the glossopharyngeal nerve and taste responses in type III taste cells. In mice lacking PKD2L1 gene, chorda tympani nerve responses to sour, but not sweet, salty, bitter, and umami tastants were reduced by 25-45% compared with those in wild type mice. In contrast, chorda tympani nerve responses in PKD1L3 knockout mice and glossopharyngeal nerve responses in single-and double-knock-out mice were similar to those in wild type mice. Sour taste responses of type III fungiform taste cells (GAD67-expressing taste cells) were also reduced by 25-45% by elimination of PKD2L1.
    Conclusions/Significance: These findings suggest that PKD2L1 partly contributes to sour taste responses in mice and that receptors other than PKDs would be involved in sour detection.

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  • Gustatory Signaling in the Periphery: Detection, Transmission, and Modulation of Taste Information 査読

    Mayu Niki, Ryusuke Yoshida, Shingo Takai, Yuzo Ninomiya

    BIOLOGICAL & PHARMACEUTICAL BULLETIN   33 ( 11 )   1772 - 1777   2010年11月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:PHARMACEUTICAL SOC JAPAN  

    Gustatory signaling begins with taste receptor cells that express taste receptors. Recent molecular biological studies have identified taste receptors and transduction components for basic tastes (sweet, salty, sour, bitter, and umami). Activation of these receptor systems leads to depolarization and an increase in [Ca2+](i), in taste receptor cells. Then transmitters are released from taste cells and activate gustatory nerve fibers. The connection between taste cells and gustatory nerve fibers would be specific because there may be only limited divergence of taste information at the peripheral transmission. Recent studies have demonstrated that sweet taste information can be modulated by hormones or other endogenous factors that could act on their receptors in a specific group of taste cells. These peripheral modulations of taste information may influence preference behavior and food intake. This paper summarizes data on molecular mechanisms for detection and transduction of taste signals in taste bud cells, information transmission from taste cells to gustatory nerve fibers, and modulation of taste signals at peripheral taste organs, in particular for sweet taste, which may play important roles in regulating energy homeostasis.

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  • Action Potential-Enhanced ATP Release From Taste Cells Through Hemichannels 査読

    Yoshihiro Murata, Toshiaki Yasuo, Ryusuke Yoshida, Kunihiko Obata, Yuchio Yanagawa, Robert F. Margolskee, Yuzo Ninomiya

    JOURNAL OF NEUROPHYSIOLOGY   104 ( 2 )   896 - 901   2010年8月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER PHYSIOLOGICAL SOC  

    Murata Y, Yasuo T, Yoshida R, Obata K, Yanagawa Y, Margolskee RF, Ninomiya Y. Action potential-enhanced ATP release from taste cells through hemichannels. J Neurophysiol 104: 896-901, 2010. First published June 2, 2010; doi: 10.1152/jn.00414.2010. Only some taste cells fire action potentials in response to sapid stimuli. Type II taste cells express many taste transduction molecules but lack well-elaborated synapses, bringing into question the functional significance of action potentials in these cells. We examined the dependence of adenosine triphosphate (ATP) transmitter release from taste cells on action potentials. To identify type II taste cells we used mice expressing a green fluorescence protein (GFP) transgene from the alpha-gustducin promoter. Action potentials were recorded by an electrode basolaterally attached to a single GFP-positive taste cell. We monitored ATP release from gustducin-expressing taste cells by collecting the electrode solution immediately after tastant-stimulated action potentials and using a luciferase assay to quantify ATP. Stimulation of gustducin-expressing taste cells with saccharin, quinine, or glutamate on the apical membrane increased ATP levels in the electrode solution; the amount of ATP depended on the firing rate. Increased spontaneous firing rates also induced ATP release from gustducin-expressing taste cells. ATP release from gustducin-expressing taste cells was depressed by tetrodotoxin and inhibited below the detection limit by carbenoxolone. Our data support the hypothesis that action potentials in taste cells responsive to sweet, bitter, or umami tastants enhance ATP release through pannexin 1, not connexin-based hemichannels.

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  • 内因性カンナビノイドはマウスの甘味応答を増大させる(Endocannabinoids enhance sweet taste sensitivities in mice) 査読

    吉田 竜介, 大栗 弾宏, 上瀧 将史, 安尾 敏明, 堀尾 奈央, 安松 啓子, 實松 敬介, 重村 憲徳, 山本 経之, Margolskee Robert F., 二ノ宮 裕三

    神経化学   49 ( 2-3 )   730 - 730   2010年8月

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    記述言語:英語   出版者・発行元:日本神経化学会  

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  • Taste Preference for Fatty Acids Is Mediated by GPR40 and GPR120 査読

    Cristina Cartoni, Keiko Yasumatsu, Tadahiro Ohkuri, Noriatsu Shigemura, Ryusuke Yoshida, Nicolas Godinot, Johannes le Coutre, Yuzo Ninomiya, Sami Damak

    JOURNAL OF NEUROSCIENCE   30 ( 25 )   8376 - 8382   2010年6月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:SOC NEUROSCIENCE  

    The oral perception of fat has traditionally been considered to rely mainly on texture and olfaction, but recent findings suggest that taste may also play a role in the detection of long chain fatty acids. The two G-protein coupled receptors GPR40 (Ffar1) and GPR120 are activated by medium and long chain fatty acids. Here we show that GPR120 and GPR40 are expressed in the taste buds, mainly in type II and type I cells, respectively. Compared with wild-type mice, male and female GPR120 knock-out and GPR40 knock-out mice show a diminished preference for linoleic acid and oleic acid, and diminished taste nerve responses to several fatty acids. These results show that GPR40 and GPR120 mediate the taste of fatty acids.

    DOI: 10.1523/JNEUROSCI.0496-10.2010

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  • Endocannabinoids selectively enhance sweet taste 査読

    Ryusuke Yoshida, Tadahiro Ohkuri, Masafumi Jyotaki, Toshiaki Yasuo, Nao Horio, Keiko Yasumatsu, Keisuke Sanematsu, Noriatsu Shigemura, Tsuneyuki Yamamoto, Robert F. Margolskee, Yuzo Ninomiya

    PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA   107 ( 2 )   935 - 939   2010年1月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:NATL ACAD SCIENCES  

    Endocannabinoids such as anandamide [N-arachidonoylethanolamine (AEA)] and 2-arachidonoyl glycerol (2-AG) are known orexigenic mediators that act via CB(1) receptors in hypothalamus and limbic forebrain to induce appetite and stimulate food intake. Circulating endocannabinoid levels inversely correlate with plasma levels of leptin, an anorexigenic mediator that reduces food intake by acting on hypothalamic receptors. Recently, taste has been found to be a peripheral target of leptin. Leptin selectively suppresses sweet taste responses in wild-type mice but not in leptin receptor-deficient db/db mice. Here, we show that endocannabinoids oppose the action of leptin to act as enhancers of sweet taste. We found that administration of AEA or 2-AG increases gustatory nerve responses to sweeteners in a concentration-dependent manner without affecting responses to salty, sour, bitter, and umami compounds. The cannabinoids increase behavioral responses to sweet-bitter mixtures and electrophysiological responses of taste receptor cells to sweet compounds. Mice genetically lacking CB(1) receptors show no enhancement by endocannnabinoids of sweet taste responses at cellular, nerve, or behavioral levels. In addition, the effects of endocannabinoids on sweet taste responses of taste cells are diminished by AM251, a CB(1) receptor antagonist, but not by AM630, a CB(2) receptor antagonist. Immunohistochemistry shows that CB(1) receptors are expressed in type II taste cells that also express the T1r3 sweet taste receptor component. Taken together, these observations suggest that the taste organ is a peripheral target of endocannabinoids. Reciprocal regulation of peripheral sweet taste reception by endocannabinoids and leptin may contribute to their opposing actions on food intake and play an important role in regulating energy homeostasis.

    DOI: 10.1073/pnas.0912048107

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  • New Frontiers in Gut Nutrient Sensor Research: Nutrient Sensors in the Gastrointestinal Tract: Modulation of Sweet Taste Sensitivity by Leptin 査読

    Nao Horio, Masafumi Jyotaki, Ryusuke Yoshida, Keisuke Sanematsu, Noriatsu Shigemura, Yuzo Ninomiya

    JOURNAL OF PHARMACOLOGICAL SCIENCES   112 ( 1 )   8 - 12   2010年1月

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    記述言語:英語   出版者・発行元:JAPANESE PHARMACOLOGICAL SOC  

    The ability to perceive sweet compounds is important for animals to detect an external carbohydrate source of calories and has a critical role in the nutritional status of animals. In mice, a subset of sweet-sensitive taste cells possesses leptin receptors. Increase of plasma leptin with increasing internal energy storage in the adipose tissue suppresses sweet taste responses via this receptor. The data from recent studies indicate that leptin may also act as a modulator of sweet taste sensation in humans with a diurnal variation in sweet sensitivity. The plasma leptin level and sweet taste sensitivity are proposed to link with post-ingestive plasma glucose level. This leptin modulation of sweet taste sensitivity may influence an individual's preference, ingestive behavior, and absorption of nutrients, thereby playing important roles in regulation of energy homeostasis.

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  • Reception and transmission of taste information in type ii and type ie taste bud cells

    Ryusuke Yoshida, Mayu Niki, Yoshihiro Murata, Noriatsu Shigemura, Yuzo Ninomiya

    Journal of Oral Biosciences   52 ( 4 )   358 - 364   2010年

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    記述言語:英語   出版者・発行元:Japanese Association for Oral Biology  

    Gustatory information processing begins with taste bud cells,astr which are activated by sapid molecules via specific taste receptors and transmit their signals to gustatory afferent fibers. Taste bud cells are morphologically classified into 4 groups (Type I -IV cells), two of which are involved in gustatory sig-naling. Type II cells express sweet, bitter, and umami taste receptors and transduction components and respond best to sweet, bitter, or umami stimuli, suggesting that sweet, bitter, and umami tastes are detected by different sets of Type II cells. Type m cells express putative sour taste receptors and respond to sour or multiple taste stimuli, indicating that sour tastes are mediated by Typem cells. These data suggest that each taste quality could be discriminated among taste bud cells. Type II cells do not possess a conventional synaptic structure but they release ATP in response to taste stimuli. Typem cells have a synaptic structure and they release serotonin and norepinephrine but not ATP. Therefore, each taste cell may use distinct mechanisms and transmitters for signal transmission to gustatory nerve fibers.

    DOI: 10.2330/joralbiosci.52.358

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  • Reciprocal modulation of sweet taste by leptin and endocannabinoids 査読

    Mayu Niki, Masafumi Jyotaki, Ryusuke Yoshida, Yuzo Ninomiya

    Results and Problems in Cell Differentiation   52   101 - 114   2010年

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Sweet taste perception is important for animals to detect carbohydrate source of calories and has a critical role in the nutritional status of animals. Recent studies demonstrated that sweet taste responses can be modulated by leptin and endocannabinoids [anandamide (N-arachidonoylethanolamine) and 2-arachidonoyl glycerol]. Leptin is an anorexigenic mediator that reduces food intake by acting on hypothalamic receptor, Ob-Rb. Leptin is shown to selectively suppress sweet taste responses in wild-type mice but not in leptin receptor-deficient db/db mice. In marked contrast, endocannabinoids are orexigenic mediators that act via CB1 receptors in hypothalamus and limbic forebrain to induce appetite and stimulate food intake. In the peripheral taste system, endocannabinoids also oppose the action of leptin and enhance sweet taste sensitivities in wild-type mice but not in mice genetically lacking CB1 receptors. These findings indicate that leptin and endocannabinoids not only regulate food intake via central nervous systems but also may modulate palatability of foods by altering peripheral sweet taste responses via their cognate receptors. © 2011 Springer Berlin Heidelberg.

    DOI: 10.1007/978-3-642-14426-4_9

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  • NEW INSIGHTS INTO THE SIGNAL TRANSMISSION FROM TASTE CELLS TO GUSTATORY NERVE FIBERS 査読

    Ryusuke Yoshida, Yuzo Ninomiya

    INTERNATIONAL REVIEW OF CELL AND MOLECULAR BIOLOGY, VOL 279   279   101 - 134   2010年

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    記述言語:英語   掲載種別:論文集(書籍)内論文   出版者・発行元:ELSEVIER ACADEMIC PRESS INC  

    Taste receptor cells detect chemical compounds in the oral cavity and transfer their messages to gustatory afferent nerve fibers. Considering the coding of taste information, the sensitivity of taste cells and the connection between taste cells and gustatory fibers may be critical in this process. Broadly tuned taste cells and random connections between taste cells and fibers would produce gustatory fibers that have broad sensitivity to multiple taste qualities. Narrowly tuned taste cells and selective connections would yield gustatory nerve fibers that respond to specific taste quality. This review summarizes results showing molecular and morphological aspects of taste bud cells, physiological responses of taste cells, possible connections between taste cells and gustatory fibers, and transmitter release from taste cells, and discusses how taste qualities are encoded among taste bud cells and how taste information is transmitted from taste cells to gustatory nerve fibers.

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  • Discrimination of taste qualities among mouse fungiform taste bud cells 査読

    Ryusuke Yoshida, Aya Miyauchi, Toshiaki Yasuo, Masafumi Jyotaki, Yoshihiro Murata, Keiko Yasumatsu, Noriatsu Shigemura, Yuchio Yanagawa, Kunihiko Obata, Hiroshi Ueno, Robert F. Margolskee, Yuzo Ninomiya

    JOURNAL OF PHYSIOLOGY-LONDON   587 ( 18 )   4425 - 4439   2009年9月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:WILEY-BLACKWELL PUBLISHING, INC  

    Multiple lines of evidence from molecular studies indicate that individual taste qualities are encoded by distinct taste receptor cells. In contrast, many physiological studies have found that a significant proportion of taste cells respond to multiple taste qualities. To reconcile this apparent discrepancy and to identify taste cells that underlie each taste quality, we investigated taste responses of individual mouse fungiform taste cells that express gustducin or GAD67, markers for specific types of taste cells. Type II taste cells respond to sweet, bitter or umami tastants, express taste receptors, gustducin and other transduction components. Type III cells possess putative sour taste receptors, and have well elaborated conventional synapses. Consistent with these findings we found that gustducin-expressing Type II taste cells responded best to sweet (25/49), bitter (20/49) or umami (4/49) stimuli, while all GAD67 (Type III) taste cells examined (44/44) responded to sour stimuli and a portion of them showed multiple taste sensitivities, suggesting discrimination of each taste quality among taste bud cells. These results were largely consistent with those previously reported with circumvallate papillae taste cells. Bitter-best taste cells responded to multiple bitter compounds such as quinine, denatonium and cyclohexamide. Three sour compounds, HCl, acetic acid and citric acid, elicited responses in sour-best taste cells. These results suggest that taste cells may be capable of recognizing multiple taste compounds that elicit similar taste sensation. We did not find any NaCl-best cells among the gustducin and GAD67 taste cells, raising the possibility that salt sensitive taste cells comprise a different population.

    DOI: 10.1113/jphysiol.2009.175075

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  • Multiple receptors underlie glutamate taste responses in mice 査読

    Keiko Yasumatsu, Nao Horio, Yoshihiro Murata, Shinya Shirosaki, Tadahiro Ohkuri, Ryusuke Yoshida, Yuzo Ninomiya

    AMERICAN JOURNAL OF CLINICAL NUTRITION   90 ( 3 )   747S - 752S   2009年9月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER SOC NUTRITION-ASN  

    L-Glutamate is known to elicit a unique taste, umami, that is distinct from the tastes of sweet, salty, sour, and bitter. Recent molecular studies have identified several candidate receptors for umami in taste cells, such as the heterodimer T1R1/T1R3 and brain-expressed and taste-expressed type 1 and 4 metabotropic glutamate receptors (brain-mGluR1, brain-mGluR4, taste-mGluR1, and taste-mGluR4). However, the relative contributions of these receptors to umami taste reception remain to be elucidated. We critically discuss data from recent studies in which mouse taste cell, nerve fiber, and behavioral responses to umami stimuli were measured to evaluate whether receptors other than T1R1/T1R3 are involved in umami responses. We particularly emphasized studies of umami responses in T1R3 knockout (KO) mice and studies of potential effects of mGluR antagonists on taste responses. The results of these studies indicate the existence of substantial residual responses to umami compounds in the T1R3-KO model and a significant reduction of umami responsiveness after administration of mGluR antagonists. These findings thus provide evidence of the involvement of mGluRs in addition to T1R1/T1R3 in umami detection in mice and suggest that umami responses, at least in mice, may be mediated by multiple receptors. Am J Clin Nutr 2009; 90(suppl): 747S-52S.

    DOI: 10.3945/ajcn.2009.27462J

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  • Variation in umami perception and in candidate genes for the umami receptor in mice and humans 査読

    Noriatsu Shigemura, Shinya Shirosaki, Tadahiro Ohkuri, Keisuke Sanematsu, A. A. Shahidul Islam, Yoko Ogiwara, Misako Kawai, Ryusuke Yoshida, Yuzo Ninomiya

    AMERICAN JOURNAL OF CLINICAL NUTRITION   90 ( 3 )   764S - 769S   2009年9月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER SOC NUTRITION-ASN  

    The unique taste induced by monosodium glutamate is referred to as umami taste. The umami taste is also elicited by the purine nucleotides inosine 5'-monophosphate and guanosine 5'-monophosphate. There is evidence that a heterodimeric G protein-coupled receptor, which consists of the T1R1 ( taste receptor type 1, member 1, Tas1r1) and the T1R3 ( taste receptor type 1, member 3, Tas1r3) proteins, functions as an umami taste receptor for rodents and humans. Splice variants of metabotropic glutamate receptors, mGluR1 ( glutamate receptor, metabotropic 1, Grm1) and mGluR4 ( glutamate receptor, metabotropic 4, Grm4), also have been proposed as taste receptors for glutamate. The taste sensitivity to umami substances varies in inbred mouse strains and in individual humans. However, little is known about the relation of umami taste sensitivity to variations in candidate umami receptor genes in rodents or in humans. In this article, we summarize current knowledge of the diversity of umami perception in mice and humans. Furthermore, we combine previously published data and new information from the single nucleotide polymorphism databases regarding variation in the mouse and human candidate umami receptor genes: mouse Tas1r1 (TAS1R1 for human), mouse Tas1r3 (TAS1R3 for human), mouse Grm1 (GRM1 for human), and mouse Grm4 (GRM4 for human). Finally, we discuss prospective associations between variation of these genes and umami taste perception in both species. Am J Clin Nutr 2009; 90( suppl): 764S-9S.

    DOI: 10.3945/ajcn.2009.27462M

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  • Genetic and Molecular Basis of Individual Differences in Human Umami Taste Perception 査読

    Noriatsu Shigemura, Shinya Shirosaki, Keisuke Sanematsu, Ryusuke Yoshida, Yuzo Ninomiya

    PLOS ONE   4 ( 8 )   2009年8月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:PUBLIC LIBRARY SCIENCE  

    Umami taste (corresponds to savory in English) is elicited by L-glutamate, typically as its Na salt (monosodium glutamate: MSG), and is one of five basic taste qualities that plays a key role in intake of amino acids. A particular property of umami is the synergistic potentiation of glutamate by purine nucleotide monophosphates (IMP, GMP). A heterodimer of a G protein coupled receptor, TAS1R1 and TAS1R3, is proposed to function as its receptor. However, little is known about genetic variation of TAS1R1 and TAS1R3 and its potential links with individual differences in umami sensitivity. Here we investigated the association between recognition thresholds for umami substances and genetic variations in human TAS1R1 and TAS1R3, and the functions of TAS1R1/TAS1R3 variants using a heterologous expression system. Our study demonstrated that the TAS1R1-372T creates a more sensitive umami receptor than -372A, while TAS1R3-757C creates a less sensitive one than - 757R for MSG and MSG plus IMP, and showed a strong correlation between the recognition thresholds and in vitro dose - response relationships. These results in human studies support the propositions that a TAS1R1/TAS1R3 heterodimer acts as an umami receptor, and that genetic variation in this heterodimer directly affects umami taste sensitivity.

    DOI: 10.1371/journal.pone.0006717

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  • NaCl RESPONSIVE TASTE CELLS IN THE MOUSE FUNGIFORM TASTE BUDS 査読

    R. Yoshida, N. Horio, Y. Murata, K. Yasumatsu, N. Shigemura, Y. Ninomiya

    NEUROSCIENCE   159 ( 2 )   795 - 803   2009年3月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:PERGAMON-ELSEVIER SCIENCE LTD  

    Previous studies have demonstrated that rodents&apos; chorda tympani (CT) nerve fibers responding to NaCl can be classified according to their sensitivities to the epithelial sodium channel (ENaC) blocker amiloride into two groups: amiloride-sensitive (AS) and -insensitive (Al). The AS fibers were shown to respond specifically to NaCl, whereas Al fibers broadly respond to various electrolytes, including NaCl. These data suggest that salt taste transduction in taste cells may be composed of at least two different systems; AS and Al ones. To further address this issue, we investigated the responses to NaCl, KCl and HCl and the amiloride sensitivity of mouse fungiform papilla taste bud cells which are innervated by the CT nerve. Comparable with the CT data, the results indicated that 56 NaCl-responsive cells tested were classified into two groups; 25 cells (similar to 44%) narrowly responded to NaCl and their NaCl response were inhibited by amiloride (AS cells), whereas the remaining 31 cells (similar to 56%) responded not only to NaCl, but to KCl and/or HCl and showed no amiloride inhibition of NaCl responses (Al cells). Amiloride applied to the basolateral side of taste cells had no effect on NaCl responses in the AS and Al cells. Single cell reverse transcription-polymerase chain reaction (RT-PCR) experiments indicated that ENaC subunit mRNA was expressed in a subset of AS cells. These findings suggest that the mouse fungiform taste bud is composed of AS and Al cells that can transmit taste information differently to their corresponding types of CT fibers, and apical ENaCs may be involved in the NaCl responses of AS cells. (C) 2009 IBRO. Published by Elsevier Ltd. All rights reserved.

    DOI: 10.1016/j.neuroscience.2008.12.052

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  • Modulation and Transmission of Sweet Taste Information for Energy Homeostasis 査読

    Keisuke Sanematsu, Nao Horio, Yoshihiro Murata, Ryusuke Yoshida, Tadahiro Ohkuri, Noriatsu Shigemura, Yuzo Ninomiya

    INTERNATIONAL SYMPOSIUM ON OLFACTION AND TASTE   1170   102 - 106   2009年

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:WILEY-BLACKWELL  

    Perception of sweet taste is important for animals to detect external energy source of calories. In mice, sweet-sensitive cells possess a leptin receptor. Increase of plasma leptin with increasing internal energy storage in the adipose tissue suppresses sweet taste responses via this receptor. Data from our recent studies indicate that leptin may also modulate sweet taste sensation in humans with a diurnal variation in sweet sensitivity. This leptin modulation of sweet taste information to the brain may influence individuals' preference and ingestive behavior, thereby playing important roles in regulation of energy homeostasis.

    DOI: 10.1111/j.1749-6632.2009.03893.x

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  • Multiple Receptor Systems for Umami Taste in Mice 査読

    Ryusuke Yoshida, Keiko Yasumatsu, Shinya Shirosaki, Masashi Jyotaki, Nao Horio, Yoshihiro Murata, Noriatsu Shigemura, Kiyohito Nakashima, Yuzo Ninomiya

    INTERNATIONAL SYMPOSIUM ON OLFACTION AND TASTE   1170   51 - 54   2009年

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:BLACKWELL PUBLISHING  

    Recent molecular studies proposed that the T2r1/T1r3 heterodimer, mGluR1 and mGluR4 might function as umami taste receptors in mice. However, the roles of each of these receptors in umami taste are not yet clear. In this paper, we summarize recent data for T1r3, mGluR1, and mGluR4 as umami taste receptors and discuss receptor systems responsible for umami detection in mice.

    DOI: 10.1111/j.1749-6632.2009.03902.x

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  • The taste transduction channel TRPM5 is a locus for bitter-sweet taste interactions 査読

    Karel Talavera, Keiko Yasumatsu, Ryusuke Yoshida, Robert F. Margolskee, Thomas Voets, Yuzo Ninomiya, Bernd Nilius

    FASEB JOURNAL   22 ( 5 )   1343 - 1355   2008年5月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:FEDERATION AMER SOC EXP BIOL  

    Ordinary gustatory experiences, which are usually evoked by taste mixtures, are determined by multiple interactions between different taste stimuli. The most studied model for these gustatory interactions is the suppression of the responses to sweeteners by the prototype bitter compound quinine. Here we report that TRPM5, a cation channel involved in sweet taste transduction, is inhibited by quinine (EC50=50 mu M at -50 mV) owing to a decrease in the maximal whole-cell TRPM5 conductance and an acceleration of channel closure. Notably, quinine inhibits the gustatory responses of sweet-sensitive gustatory nerves in wildtype (EC50=similar to 1.6 mM) but not in Trpm5 knockout mice. Quinine induces a dose- and time-dependent inhibition of TRPM5-dependent responses of single sweet-sensitive fibers to sucrose, according to the restricted diffusion of the drug into the taste tissue. Quinidine, the stereoisomer of quinine, has similar effects on TRPM5 currents and on sweet-induced gustatory responses. In contrast, the chemically unrelated bitter compound denatonium benzoate has an similar to 100-fold weaker effect on TRPM5 currents and, accordingly, at 10 mM it does not alter gustatory responses to sucrose. The inhibition of TRPM5 by bitter compounds constitutes the molecular basis of a novel mechanism of taste interactions, whereby the bitter tastant inhibits directly the sweet transduction pathway.

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  • Amiloride-sensitive NaCl taste responses are associated with genetic variation of ENaC alpha-subunit in mice 査読

    Noriatsu Shigemura, Tadahiro Ohkuri, Chiharu Sadamitsu, Keiko Yasumatsu, Ryusuke Yoshida, Gary K. Beauchamp, Alexander A. Bachmanov, Yuzo Ninomiya

    AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY   294 ( 1 )   R66 - R75   2008年1月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER PHYSIOLOGICAL SOC  

    An epithelial Na+ channel (ENaC) is expressed in taste cells and may be involved in the salt taste transduction. ENaC activity is blocked by amiloride, which in several mammalian species also inhibits taste responses to NaCl. In mice, lingual application of amiloride inhibits NaCl responses in the chorda tympani (CT) gustatory nerve much stronger in the C57BL/6 (B6) strain than in the 129P3/J (129) strain. We examined whether this strain difference is related to gene sequence variation or mRNA expression of three ENaC subunits (alpha, beta, gamma). Real-time RT-PCR and in situ hybridization detected no significant strain differences in expression of all three ENaC subunits in fungiform papillae. Sequences of the beta- and gamma ENaC subunit genes were also similar in the B6 and 129 strains, but alpha ENaC gene had three single nucleotide polymorphisms (SNPs). One of these SNPs resulted in a substitution of arginine in the B6 strain to tryptophan in the 129 strain (R616W) in the alpha ENaC protein. To examine association of this SNP with amiloride sensitivity of CT responses to NaCl, we produced F2 hybrids between B6 and 129 strains. Amiloride inhibited CT responses to NaCl in F-2 hybrids with B6/129 and B6/B6 alpha ENaC R616W genotypes stronger than in F-2 hybrids with 129/129 genotype. This suggests that the R616W variation in the alpha ENaC subunit affects amiloride sensitivity of the ENaC channel and provides evidence that ENaC is involved in amiloride-sensitive salt taste responses in mice.

    DOI: 10.1152/ajpregu.00420.2007

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  • Abnormal taste perception in mice lacking the type 3 inositol 1,4,5-trisphosphate receptor 査読

    Chihiro Hisatsune, Keiko Yasumatsu, Hiromi Takahashi-Iwanaga, Naoko Ogawa, Yukiko Kuroda, Ryusuke Yoshida, Yuzo Ninomiya, Katsuhiko Mikoshiba

    JOURNAL OF BIOLOGICAL CHEMISTRY   282 ( 51 )   37225 - 37231   2007年12月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC  

    Inositol 1,4,5-trisphosphate receptor (IP3R) is one of the important calcium channels expressed in the endoplasmic reticulum and has been shown to play crucial roles in various physiological phenomena. Type 3 IP3R is expressed in taste cells, but the physiological relevance of this receptor in taste perception in vivo is still unknown. Here, we show that mice lacking IP(3)R3 show abnormal behavioral and electrophysiological responses to sweet, umami, and bitter substances that trigger G-protein-coupled receptor activation. In contrast, responses to salty and acid tastes are largely normal in the mutant mice. We conclude that IP3R3 is a principal mediator of sweet, bitter, and umami taste perception and would be a missing molecule linking phospholipase C beta 2 to TRPM5 activation.

    DOI: 10.1074/jbc.M705641200

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  • Glutamate responses of mouse fungiform taste cells with action potentials 査読

    Yoshihiro Murata, Ryusuke Yoshida, Toshiaki Yasuo, Keiko Yasumatsu, Noriatsu Shigemura, Yuzo Ninomiya

    NEUROSCIENCE RESEARCH   58   S217 - S217   2007年

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    記述言語:英語   出版者・発行元:ELSEVIER IRELAND LTD  

    DOI: 10.1016/j.neures.2007.06.1001

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  • Taste receptor cells generating action potentials within a single taste bud of mouse fungiform papillae 査読

    Ryusuke Yoshida, Yoshihiro Murata, Toshiaki Yasuo, Keiko Yasumatsu, Noriatsu Shigemura, Yuzo Ninomiya

    NEUROSCIENCE RESEARCH   58   S217 - S217   2007年

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    記述言語:英語   出版者・発行元:ELSEVIER IRELAND LTD  

    DOI: 10.1016/j.neures.2007.06.1002

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  • Coding channels for taste perception: information transmission from taste cells to gustatory nerve fibers 査読

    Ryusuke Yoshida, Keiko Yasumatsu, Noriatsu Shigemura, Yuzo Ninomiya

    ARCHIVES OF HISTOLOGY AND CYTOLOGY   69 ( 4 )   233 - 242   2006年12月

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    記述言語:英語   出版者・発行元:INT SOC HISTOLOGY & CYTOLOGY  

    Taste signals are first detected by the taste receptor cells, which are located in taste buds existing in the tongue, soft palate, larynx and epiglottis. Taste receptor cells contact with the chemical compounds in oral cavity through the apical processes which protrude into the taste pore. Interaction between chemical compounds and the taste receptor produces activation of taste receptor cells directly or indirectly. Then the signals are transmitted to gustatory nerve fibers and higher order neurons. A recent study demonstrated many similarities between response properties of taste receptor cells with action potentials and those of the gustatory nerve fibers innervating them, suggesting information derived from receptor cells generating action potentials may form a major component of taste information that is transmitted to gustatory nerve fibers. These findings may also indicate that there is no major modification of taste information sampled by taste receptor cells in synaptic transmission from taste cells to nerve fibers although there is indirect evidence. In the peripheral taste system, gustatory nerve fibers may selectively contact with taste receptor cells that have similar response properties and convey constant taste information to the higher order neurons.

    DOI: 10.1679/aohc.69.233

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  • Taste responsiveness of fungiform taste cells with action potentials 査読

    Ryusuke Yoshida, Noriatsu Shigemura, Keisuke Sanematsu, Keiko Yasumatsu, Satoru Ishizuka, Yuzo Ninomiya

    JOURNAL OF NEUROPHYSIOLOGY   96 ( 6 )   3088 - 3095   2006年12月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER PHYSIOLOGICAL SOC  

    It is known that a subset of taste cells generate action potentials in response to taste stimuli. However, responsiveness of these cells to particular tastants remains unknown. In the present study, by using a newly developed extracellular recording technique, we recorded action potentials from the basolateral membrane of single receptor cells in response to taste stimuli applied apically to taste buds isolated from mouse fungiform papillae. By this method, we examined taste-cell responses to stimuli representing the four basic taste qualities (NaCl, Na saccharin, HCl, and quinine-HCl). Of 72 cells responding to taste stimuli, 48 (67%) responded to one, 22 (30%) to two, and 2 (3%) to three of four taste stimuli. The entropy value presenting the breadth of responsiveness was 0.158 +/- 0.234 (mean +/- SD), which was close to that for the nerve fibers (0.183 +/- 0.262). In addition, the proportion of taste cells predominantly sensitive to each of the four taste stimuli, and the grouping of taste cells based on hierarchical cluster analysis, were comparable with those of chorda tympani (CT) fibers. The occurrence of each class of taste cells with different taste responsiveness to the four taste stimuli was not significantly different from that of CT fibers except for classes with broad taste responsiveness. These results suggest that information derived from taste cells generating action potentials may provide the major component of taste information that is transmitted to gustatory nerve fibers.

    DOI: 10.1152/jn.00409.2006

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  • Amiloride inhibition on NaCl responses of the chorda tympani nerve in two 129 substrains of mice, 129P3/J and 129X1/SvJ 査読

    Tadahiro Ohkuri, Keiko Yasumatsu, Noriatsu Shigemura, Ryusuke Yoshida, Yuzo Ninomiya

    CHEMICAL SENSES   31 ( 6 )   565 - 572   2006年7月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:OXFORD UNIV PRESS  

    Amiloride, a sodium channel blocker, is known to suppress NaCl responses of the chorda tympani (CT) nerve in various mammalian species. In mice, the NaCl suppressing effect of amiloride is reported to differ among strains. In C57BL mice, amiloride inhibits NaCl responses to about 50% of control, whereas no such clear suppression was evident in prior studies with 129 mice. However, evidence from behavioral studies is not entirely consistent with this. Recently, it has been found that genetic backgrounds of 129 mice differ within substrains. 129X1/SvJ (formerly 129/SvJ) mice differ from the 129P3/J (formerly 129/J) strain by 25% of sequence length polymorphisms. Therefore, we examined possible substrain difference between 129P3/J and 129X1/SvJ mice in the amiloride sensitivity of electrophysiologically. recorded NaCl responses. Amiloride significantly suppressed CT responses to NaCl without affecting responses to KCl both in 129P3/J and 129X1/SvJ mice. However, the magnitude of the amiloride inhibition was significantly larger (similar to 50% of control in response to 0.01-1.0 M NaCl by 100 mu M amiloride) in 129X1/SvJ than in 129P3/J mice (similar to 20% of control in response to 0.03-0.3 M NaCl by 100 mu M amiloride). Threshold amiloride concentration for suppression of responses to 0.3 M NaCl was 30 mu M in 129P3/J mice, which was higher than that in 129X1/SvJ mice (10 mu M). In 129X1/SvJ mice, the threshold amiloride concentration eliciting inhibition of NaCl responses and the magnitude of the inhibition were comparable with those in C57BL/6 mice. These results suggest that amiloride sensitivity of NaCl responses differs even among the 129 substrains, 129P3/J and 129 X1/SvJ, and the substrain difference of 129 mice in amiloride sensitivity is as large as that between two inbred strains (129P3/J and C57BL/6).

    DOI: 10.1093/chemse/bjj061

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  • Trpm5 null mice respond to bitter, sweet, and umami compounds 査読

    S Damak, MQ Rong, K Yasumatsu, Z Kokrashvili, CA Perez, N Shigemura, R Yoshida, B Mosinger, JI Glendinning, Y Ninomiya, RF Margolskee

    CHEMICAL SENSES   31 ( 3 )   253 - 264   2006年3月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:OXFORD UNIV PRESS  

    Trpm5 is a calcium-activated cation channel expressed selectively in taste receptor cells. A previous study reported that mice with an internal deletion of Trpm5, lacking exons 15-19 encoding transmembrane segments 1-5, showed no taste-mediated responses to bitter, sweet, and umami compounds. We independently generated knockout mice null for Trpm5 protein expression due to deletion of Trpm5's promoter region and exons 1-4 (including the translation start site). We examined the taste-mediated responses of Trpm5 null mice and wild-type (WT) mice using three procedures: gustatory nerve recording [chorda tympani (CT) and glossopharyngeal (NG) nerves], initial lick responses, and 24-h two-bottle preference tests. With bitter compounds, the Trpm5 null mice showed reduced, but not abolished, avoidance (as indicated by licking responses and preference ratios higher than those of WT), a normal CT response, and a greatly diminished NG response. With sweet compounds, Trpm5 null mice showed no licking response, a diminished preference ratio, and absent or greatly reduced nerve responses. With umami compounds, Trpm5 null mice showed no licking response, a diminished preference ratio, a normal NG response, and a greatly diminished CT response. Our results demonstrate that the consequences of eliminating Trmp5 expression vary depending upon the taste quality and the lingual taste field examined. Thus, while Trpm5 is an important factor in many taste responses, its absence does not eliminate all taste responses. We conclude that Trpm5-dependent and Trpm5-independent pathways underlie bitter, sweet, and umami tastes.

    DOI: 10.1093/chemse/bjj027

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  • Mouse strain differences in gurmarin-sensitivity of sweet taste responses are not associated with polymorphisms of the sweet receptor gene, Tas1r3 査読

    K Sanematsu, K Yasumatsu, R Yoshida, N Shigemura, Y Ninomiya

    CHEMICAL SENSES   30 ( 6 )   491 - 496   2005年7月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:OXFORD UNIV PRESS  

    Gurmarin (Gur) is a peptide that selectively inhibits responses of the chorda tympani (CT) nerve to sweet compounds in rodents. In mice, the sweet-suppressing effect of Gur differs among strains. The inhibitory effect of Gur is clearly observed in C57BL/6 mice, but only slightly, if at all, in BALB/c mice. These two mouse strains possess different alleles of the sweet receptor gene, Sac (Tas1r3) (taster genotype for C57BL/6 and non-taster genotype for BALB/c mice), suggesting that polymorphisms in the gene may account for differential sensitivity to Gur. To investigate this possibility, we examined the effect of Gur in another Tas1r3 non-taster strain, 129X1/Sv mice. The results indicated that unlike non-taster BALB/c mice but similar to taster C57BL/6 mice, 129X1/Sv mice exhibited significant inhibition of CT responses to various sweet compounds by Gur. This suggests that the mouse strain difference in the Gur inhibition of sweet responses of the CT nerve may not be associated with polymorphisms of Tas1r3.

    DOI: 10.1093/chemse/bji041

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  • Expression of amiloride-sensitive epithelial sodium channels in mouse taste cells after chorda tympani nerve crush 査読

    N Shigemura, AAS Islam, C Sadamitsu, R Yoshida, K Yasumatsu, Y Ninomiya

    CHEMICAL SENSES   30 ( 6 )   531 - 538   2005年7月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:OXFORD UNIV PRESS  

    Our previous electrophysiological study demonstrated that amiloride-sensitive (AS) and -insensitive (AI) components of NaCl responses recovered differentially after the mouse chorda tympani (CT) was crushed. AI responses reappeared earlier (at 3 weeks after the nerve crush) than did AS ones (at 4 weeks). This and other results suggested that two salt-responsive systems were differentially and independently reformed after nerve crush. To investigate the molecular mechanisms of formation of the salt responsive systems, we examined expression patterns of three subunits (alpha, beta and gamma) of the amiloride-sensitive epithelial Na+ channel (ENaC) in mouse taste cells after CT nerve crush by using in situ hybridization (ISH) analysis. The results showed that all three ENaC subunits, as well as alpha-gustducin, a marker of differentiated taste cells, were expressed in a subset of taste bud cells from an early stage (1-2 weeks) after nerve crush, although these taste buds were smaller and fewer in number than for control mice. At 3 weeks, the mean number of each ENaC subunit and alpha-gustducin mRNA-positive cells per taste bud reached the control level. Also, the size of taste buds became similar to those of the control mice at this time. Our previous electrophysiological study demonstrated that at 2 weeks no significant response of the nerve to chemical stimuli was observed. Thus ENaC subunits appear to be expressed prior to the reappearance of AI and AS neural responses after CT nerve crush. These results support the view that differentiation of taste cells into AS or AI cells is initiated prior to synapse formation.

    DOI: 10.1093/chemse/bji046

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  • The role of the dpa locus in mice 査読

    N Shigemura, K Yasumatsu, R Yoshida, N Sako, H Katsukawa, K Nakashima, T Imoto, Y Ninomiya

    CHEMICAL SENSES   30   I84 - i85   2005年1月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:OXFORD UNIV PRESS  

    DOI: 10.1093/chemse/bjh125

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  • Taste receptor cells responding with action potentials to taste stimuli and their molecular expression of taste related genes 査読

    R Yoshida, K Sanematsu, N Shigemura, K Yasumatsu, Y Ninomiya

    CHEMICAL SENSES   30   I19 - i20   2005年1月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:OXFORD UNIV PRESS  

    DOI: 10.1093/chemse/bjh092

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  • Recovery of salt taste responses and PGP 9.5 immunoreactive taste bud cells during regeneration of the mouse chorda tympani nerve 査読

    K Yasumatsu, N Shigemura, R Yoshida, Y Ninomiya

    CHEMICAL SENSES   30   I62 - i63   2005年1月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:OXFORD UNIV PRESS  

    DOI: 10.1093/chemse/bjh114

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  • Search for cerebral G cluster neurons responding to taste stimulation with seaweed in Aplysia kurodai by the use of calcium imaging 査読

    R Yoshida, T Nagahama

    JOURNAL OF NEUROBIOLOGY   55 ( 3 )   299 - 314   2003年6月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:JOHN WILEY & SONS INC  

    The calcium imaging method can detect the spike activities of many neurons simultaneously. In the present experiments, this method was used to search for unique neurons contributing to feeding behavior in the cerebral ganglia of Aplysia kurodai. We mainly explored the neurons whose cell bodies were located in the G cluster and the neuropile region posterior to this cluster on the ventral surface of the cerebral ganglia. When the extract of the food seaweed Ulva was applied to the tentacle-lip region, many neurons stained with a calcium-sensitive dye, Calcium Green-1, showed changes in fluorescence. Some neurons showed rhythmic responses and others showed transient responses, suggesting that these neurons may be partly involved in the feeding circuits. We also identified three motor neurons among these neurons that showed rhythmic fluorescence responses to the taste stimulation. One of them was a motor neuron shortening the anterior tentacle (ATS), and the other two were motor neurons producing lip opening-like (LOG) and closing-like (LCG) movements, respectively. Application of the Ulva extract to the tentacle-lip region induced phase-locked rhythmic firing activity in these motor neurons, suggesting that these neurons may contribute to the rhythmic patterned movements of the anterior tentacles and lips during the ingestion of seaweed. (C) 2003 Wiley Periodicals, Inc.

    DOI: 10.1002/neu.10207

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  • 【分子を感じる 感覚の分子生物学】味を感じる:神経メカニズム

    安松 啓子, 三浦 裕仁, 吉田 竜介, 日野 明寛, 二ノ宮 裕三

    細胞工学   21 ( 12 )   1429 - 1433   2002年11月

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    記述言語:日本語   出版者・発行元:(株)学研メディカル秀潤社  

    味を受容する味蕾は,味細胞が数十個集まってできている.味細胞の寿命は短く,約10日のサイクルで,新しく置き換わっている(ターンオーバー).味神経は味蕾の基底部にsonic hedgehog(Shh)を誘導し味細胞を増殖し,味蕾を維持するものと推定される.味神経線維は各々適合する特定の味細胞或いはその前駆細胞を選択し,シナプスを作り,ターンオーバーに際しても味の情報を変えることなく脳に伝える

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  • Calcium imaging for detection and estimation of spike activities in Aplysia neurons 査読

    R Yoshida, A Iwamoto, T Nagahama

    ZOOLOGICAL SCIENCE   18 ( 5 )   631 - 643   2001年7月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:ZOOLOGICAL SOC JAPAN  

    We explored whether the calcium imaging can be applicable to detection of spike activity of Aplysia wide-spread neurons. Well-used procedures, the membrane permeable acetoxymethyl (AM) types and the retrograde labeling could not be used for loading the calcium sensitive dye into many neurons, however, impalement of each cell body with a microelectrode containing high concentration of the dye solution in turn could load the dye iontophoretically into many large neurons in a relatively short time and into several small neurons in a very short time. Spike activity just induced a fluorescent increase in the cell body while depolarization without spikes induced it in the axon hillock. In the cell body the slope of the fluorescent increase was almost relative to the spike frequency while the period of it almost corresponded to the firing duration. Therefore, the phase relationship of the rhythmic firing responses in plural neurons could be precisely detected. Moreover stable responses could be repeatedly obtained for a long time from small neurons unsuitable for a long time recording with microelectrodes. Removal of the extracellular Ca2+ completely suppressed the spike-induced increase in fluorescence in the cell body and application of nifedipine partly reduced it, suggesting contribution of L-type channels distributing in Aplysia wide-spread neurons.

    DOI: 10.2108/zsj.18.631

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書籍等出版物

  • Sweet and Umami Taste「The Senses: A Comprehensive Reference, Reference Work, 2nd Edition」

    Ryusuke Yoshida, Yuzo Ninomiya

    Elsevier  2020年9月 

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  • 味蕾

    吉田竜介( 担当: 単著)

    脳科学辞典:日本神経科学学会  2018年4月 

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  • レプチンによる甘味感受性調節機構 「おいしさの科学的評価・測定法と応用展開」

    吉田竜介, 二ノ宮裕三( 範囲: 63-74)

    CMC出版  2016年9月 

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  • Peptide Signaling in Taste Transduction. 「Chemosensory Transduction: The Detection of Odors, Tastes, and Other Chemostimuli.」

    Takai S, Yoshida R, Shigemura N, Ninomiya Y

    Academic Press  2016年2月 

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  • マウス味細胞応答記録法「研究者が教える動物実験・第1巻・感覚」

    吉田竜介

    共立出版  2015年7月 

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  • 味覚「アミノ酸科学の最前線」

    吉田竜介

    CMC出版  2015年5月 

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  • 味覚「基礎歯科生理学第6版」

    吉田竜介, 二ノ宮裕三

    医歯薬出版  2014年2月 

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  • マウス「研究者が教える動物飼育-第3巻-」

    吉田竜介( 範囲: 154-158)

    共立出版  2012年5月 

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MISC

  • アドレノメデュリンによるT1Rs非依存性経路を介するマウス鼓索神経甘味応答増強効果

    岩田周介, 岩田周介, 井上真由子, 吉田竜介, 重村憲徳, 二ノ宮裕三, 二ノ宮裕三

    Journal of Oral Biosciences Supplement (Web)   2020   2020年

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  • Roles of sugar transporters and calorie sensors in taste cells

    Yuzo Ninomiya, Keiko Yasumatsu (Nakano), Ryusuke Yoshida, Shusuke Iwata, Shigemura Noriatsu

    CHEMICAL SENSES   44 ( 3 )   E13 - E13   2019年3月

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:OXFORD UNIV PRESS  

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  • アドレノメデュリンによるT1Rs非依存性経路を介するマウス鼓索神経糖応答への影響

    岩田周介, 岩田周介, 井上真由子, 吉田竜介, 二ノ宮裕三, 二ノ宮裕三

    Journal of Oral Biosciences Supplement (Web)   2019   397 (WEB ONLY)   2019年

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    記述言語:日本語  

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  • アドレノメデュリンによるマウス鼓索神経応答への影響

    岩田 周介, 安松 啓子, 吉田 竜介, 二ノ宮 裕三

    Journal of Oral Biosciences Supplement   2018   396 - 396   2018年9月

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    記述言語:日本語   出版者・発行元:(一社)歯科基礎医学会  

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  • アンジオテンシンIIのT1Rs非依存的甘味応答に及ぼす影響

    岩田 周介, 安松 啓子, 井上 真由子, 吉田 竜介, 重村 憲徳, 二ノ宮 裕三

    日本味と匂学会誌   ( 第51回大会Proceeding集 )   S31 - S34   2017年9月

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    記述言語:日本語   出版者・発行元:日本味と匂学会  

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  • Gustatory responses of taste receptor cells expressing fluorescent proteins in transgenic mice

    Ryusuke Yoshida, Keiko Yasumatsu-Nakano, Keisuke Sanematsu, Noriatsu Shigemura, Yuzo Ninomiya

    CHEMICAL SENSES   41 ( 9 )   E115 - E115   2016年11月

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:OXFORD UNIV PRESS  

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  • Glucagon like peptide-1, sweet taste and metabolic modulation of peripheral taste information

    Shingo Takai, Noriatsu Shigemura, Keiko Yasumatsu-Nakano, Mayuko Inoue, Shusuke Iwata, Ryusuke Yoshida, Robert F. Margolskee, Yuzo Ninomiya

    CHEMICAL SENSES   41 ( 9 )   E128 - E128   2016年11月

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:OXFORD UNIV PRESS  

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  • Intracellular acidification is involved in full activation of the sweet taste receptor by miraculin

    Keisuke Sanematsu, Masayuki Kitagawa, Ryusuke Yoshida, Satoru Nirasawa, Noriatsu Shigemura, Yuzo Ninomiya

    CHEMICAL SENSES   41 ( 9 )   E276 - E276   2016年11月

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:OXFORD UNIV PRESS  

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  • 味覚と健康 栄養素センサー研究の現状と未来 味覚受容体の機能(塩味と甘味)

    重村 憲徳, 吉田 竜介, 安松 啓子, 大栗 弾宏, 岩田 周介, 高井 信吾, 上瀧 将史, 仁木 麻由, 實松 敬介, 二ノ宮 祐三

    日本薬学会年会要旨集   136年会 ( 1 )   206 - 206   2016年3月

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    記述言語:日本語   出版者・発行元:(公社)日本薬学会  

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  • The function of glucagon-like peptide-1 in the mouse peripheral taste system

    Shingo Takai, Ryusuke Yoshida, Keiko Yasumatsu, Noriatsu Shigemura, Yuzo Ninomiya

    Journal of Oral Biosciences   58 ( 1 )   10 - 15   2016年2月

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    掲載種別:書評論文,書評,文献紹介等  

    © 2015 Japanese Association for Oral Biology. Published by Elsevier B.V. All rights reserved. Background Several studies have demonstrated that some gut peptides known to be important in energy metabolism are expressed in mouse taste bud cells. However, the functions of these peptides in taste cells are still largely unknown. In the gut, one of these peptides, glucagon-like peptide-1 (GLP-1), which is known as the insulinotropic gut peptide, is secreted from enteroendocrine L-cells, which express as many taste molecules as those on the tongue. These taste transduction molecules are suggested to be involved in GLP-1 secretion from L-cells in response to various nutrient stimuli. GLP-1 is reported to function as a neurotransmitter via activation of its receptors expressed on the vagus nerve, thereby regulating insulin secretion. Highlight Consistent with this evidence from the gastrointestinal tract, recent studies have demonstrated that GLP-1 is secreted from mouse taste cells in response to taste compounds such as sugars, artificial sweeteners, and long-chain fatty acids. GLP-1 secreted from taste cells may activate particular types of gustatory nerve fibers because they express GLP-1 receptors and respond to GLP-1 administered via the femoral vein. Conclusion GLP-1 released from taste cells may be involved in transmission of sweet and lipid signals, thereby impacting animalsfeeding behavior in response to these important nutrient factors.

    DOI: 10.1016/j.job.2015.09.002

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  • ホルモンによる味覚(塩味・甘味)感受性調節

    重村 憲徳, 吉田 竜介, 安松 啓子, 大栗 弾宏, 岩田 周介, 高井 信吾, 上瀧 将史, 仁木 麻由, 實松 敬介, 二ノ宮 裕三

    日本生物工学会大会講演要旨集   平成27年度   161 - 161   2015年9月

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    記述言語:日本語   出版者・発行元:(公社)日本生物工学会  

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  • 口腔生理学分野の研究最前線Frontier in the field of Oral Physiology エンドカンナビノイドによる自己増幅的甘味増強とT1R3-非依存的甘味受容経路の存在

    岩田 周介, 吉田 竜介, 重村 憲徳, 二ノ宮 裕三

    Journal of Oral Biosciences Supplement   2015   115 - 115   2015年9月

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    記述言語:日本語   出版者・発行元:(一社)歯科基礎医学会  

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  • 味細胞におけるエンドカンナビノイドを介した甘味応答の自己増幅

    岩田 周介, 吉田 竜介, 重村 憲徳, 二ノ宮 裕三

    Journal of Oral Biosciences Supplement   2015   295 - 295   2015年9月

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    記述言語:日本語   出版者・発行元:(一社)歯科基礎医学会  

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  • Involvement of CCK in normal gustatory responses to bitter compounds

    Misa Shin, Keiko Yasumatsu, Shingo Takai, Noriatsu Shigemura, Ryusuke Yoshida, Soichi Takiguchi, Seiji Nakamura, Yuzo Ninomiya

    CHEMICAL SENSES   40 ( 3 )   259 - 260   2015年3月

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:OXFORD UNIV PRESS  

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  • 【香辛料の味修飾作用及び消化管を介した代謝調節作用】ホルモンによる味覚修飾と摂食調節 アンジオテンシンIIと味覚

    重村 憲徳, 吉田 竜介, 安松 啓子, 大栗 弾宏, 岩田 周介, 高井 信吾, 上瀧 将史, 仁木 麻由, 實松 敬介, 二ノ宮 裕三

    日本味と匂学会誌   21 ( 1 )   49 - 53   2014年4月

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    記述言語:日本語   出版者・発行元:日本味と匂学会  

    アンジオテンシンIIは、視床下部、副腎や血管などに発現するAT1受容体を介して、血圧や体内Na+濃度を調節する鍵ホルモンとして知られている。我々は、このアンジオテンシンIIが末梢の味覚器にも働き、塩味感受性を低下させNaCl溶液の摂取量を増加させること、さらに甘味感受性を増強することで糖分摂取にも影響することを明らかにした。この"味覚を介したNa+/糖ホメオスタシス維持機構"のさらなる解明は、高血圧や肥満・糖尿病などの生活習慣病に対する新たな予防・治療法の開発"に繋がることが期待される。(著者抄録)

    DOI: 10.18965/tasteandsmell.21.1_49

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  • Involvement of multiple populations of taste cells and afferent neurons in umami taste detection

    Y. Ninomiya, K. Yasumatsu, R. Yoshida

    CHEMICAL SENSES   39 ( 1 )   77 - 77   2014年1月

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:OXFORD UNIV PRESS  

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  • 味蕾から分泌される消化管ホルモンは味質特異的な情報伝達に関与する

    高井信吾, 安松啓子, 岩田周介, 井上真由子, 吉田竜介, 重村憲徳, DRUCKER Daniel J, MARGOLSKEE Robert F, 二ノ宮裕三, 二ノ宮裕三

    Journal of Oral Biosciences Supplement (Web)   2014   ROMBUNNO.SS11‐1 (WEB ONLY)   2014年

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    記述言語:日本語  

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  • Endogenous humoral modulators of behavioral preference for sweet and salty tastes

    Yuzo Ninomiya, Mayu Niki, Ryusuke Yoshida, Noriatsu Shigemura

    JOURNAL OF PHYSIOLOGICAL SCIENCES   63   S59 - S59   2013年

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:SPRINGER JAPAN KK  

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  • レプチン受容体アンタゴニストによるマウスの甘味応答

    仁木 麻由, 上瀧 将史, 吉田 竜介, 二ノ宮 裕三

    日本味と匂学会誌 = The Japanese journal of taste and smell research   18 ( 3 )   255 - 258   2011年12月

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    記述言語:日本語   出版者・発行元:日本味と匂学会  

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    その他リンク: http://search.jamas.or.jp/link/ui/2012174177

  • The taste organ is a target for orexigenic and anorexic mediators

    Yuzo Ninomiya, Mayu Niki, Tadahiro Ohkuri, Masafumi Jyotaki, Ryusuke Yoshida

    CHEMICAL SENSES   36 ( 1 )   E2 - E2   2011年1月

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:OXFORD UNIV PRESS  

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  • Modulation of sweet sensitivity by endogenous leptin and endocannabinoid

    Mayu Niki, Masafumi Jyotaki, Tadahiro Ohkuri, Ryusuke Yoshida, Yuzo Ninomiya

    NEUROSCIENCE RESEARCH   71   E163 - E163   2011年

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:ELSEVIER IRELAND LTD  

    DOI: 10.1016/j.neures.2011.07.703

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  • Involvement of mGluRs in umami detection in mice

    Yoko Kusuhara, Keiko Yasumatsu, Tadahiro Ohkuri, Ryusuke Yoshida, Katsumasa Maeda, Yuzo Ninomiya

    NEUROSCIENCE RESEARCH   71   E358 - E358   2011年

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:ELSEVIER IRELAND LTD  

    DOI: 10.1016/j.neures.2011.07.1569

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  • Humoral modulation of sweet taste sensitivities for energy homeostasis

    Yuzo Ninomiya, Mayu Niki, Masafumi Jyotaki, Tadahiro Ohkuri, Ryusuke Yoshida

    NEUROSCIENCE RESEARCH   71   E40 - E41   2011年

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:ELSEVIER IRELAND LTD  

    DOI: 10.1016/j.neures.2011.07.179

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  • Expression of G alpha subunits in sweet and umami taste cells in mice

    Ryusuke Yoshida, Aya Miyauchi, Robert F. Margolskee, Yuzo Ninomiya

    NEUROSCIENCE RESEARCH   71   E154 - E154   2011年

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:ELSEVIER IRELAND LTD  

    DOI: 10.1016/j.neures.2011.07.665

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  • マウス味細胞の味応答時におけるGABAの作用

    安尾 敏明, 吉田 竜介, 柳川 右千夫, MARGOLSKEE Robert F, 二ノ宮 裕三

    日本味と匂学会誌 = The Japanese journal of taste and smell research   17 ( 3 )   227 - 230   2010年12月

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    記述言語:日本語   出版者・発行元:日本味と匂学会  

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  • マウス味細胞の味応答に対するGABAの影響

    安尾敏明, 吉田竜介, 重村憲徳, 柳川右千夫, 二ノ宮裕三

    Journal of Oral Biosciences   52 ( Supplement )   100   2010年9月

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    記述言語:日本語  

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  • 味蕾内におけるGABAの応答特性

    安尾敏明, 吉田竜介, 堀尾奈央, 重村憲徳, 二ノ宮裕三

    日本生理学雑誌   72 ( 2 )   43   2010年2月

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  • GABA act as a modulator for sweet and bitter taste responses of mice taste bud cells

    Toshiaki Yasuo, Ryusuke Yoshida, Noriatsu Shigemura, Robert Margolskee, Yuzo Ninomiya

    JOURNAL OF PHYSIOLOGICAL SCIENCES   60   S143 - S143   2010年

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:SPRINGER TOKYO  

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  • Endocannabinoids enhance sweet taste sensitivities in mice

    Ryusuke Yoshida, Tadahiro Ohkuri, Masafumi Jyotaki, Toshiaki Yasuo, Nao Horio, Keiko Yasumatsu, Keisuke Sanematsu, Noriatsu Shigemura, Tsuneyuki Yamamoto, Robert F. Margolskee, Yuzo Ninomiya

    NEUROSCIENCE RESEARCH   68   E389 - E390   2010年

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:ELSEVIER IRELAND LTD  

    DOI: 10.1016/j.neures.2010.07.1726

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  • GABA influence on taste cell responses in mice

    Toshiaki Yasuo, Ryusuke Yoshida, Noriatsu Shigemura, Robert F. Margolskee, Yuzo Ninomiya

    NEUROSCIENCE RESEARCH   68   E384 - E384   2010年

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:ELSEVIER IRELAND LTD  

    DOI: 10.1016/j.neures.2010.07.1702

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  • Single nucleotide polymorphisms (SNP) in taste sensor genes and perceptual diversity

    Noriatsu Shigemura, Yoko Ogiwara, Keisuke Sanematsu, Misako Kawai, Ryusuke Yoshida, Yuzo Ninomiya

    JOURNAL OF PHYSIOLOGICAL SCIENCES   60   S73 - S73   2010年

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:SPRINGER TOKYO  

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  • PKD2L1 is associated with the sour taste transduction

    Nao Horio, Ryusuke Yoshida, Keiko Yasumatsu, Yuchio Yanagawa, Yoshiro Ishimaru, Hiroaki Matsunami

    NEUROSCIENCE RESEARCH   68   E385 - E385   2010年

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    DOI: 10.1016/j.neures.2010.07.1703

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  • マウス味細胞におけるGABAの機能解析

    安尾 敏明, 吉田 竜介, 堀尾 奈央, 重村 憲徳, 二ノ宮 裕三

    日本味と匂学会誌 = The Japanese journal of taste and smell research   16 ( 3 )   323 - 326   2009年12月

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    記述言語:日本語   出版者・発行元:日本味と匂学会  

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  • Different Response Properties between Type II and Type III Taste Bud Cells in Mouse Fungiform Papillae

    Ryusuke Yoshida, Toshiaki Yasuo, Yoshihiro Murata, Masashi Jyotaki, Yuchio Yanagawa, Kunihiko Obata, Hiroshi Ueno, Robert F. Margolskee, Yuzo Ninomiya

    CHEMICAL SENSES   34 ( 7 )   A72 - A72   2009年9月

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:OXFORD UNIV PRESS  

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  • Genetic and Molecular Basis of Individual Differences in Human Umami Taste Perception

    Noriatsu Shigemura, Shinya Shirosaki, Keisuke Sanematsu, Yoko Ogiwara, Misako Kawai, Ryusuke Yoshida, Yuzo Ninomiya

    CHEMICAL SENSES   34 ( 7 )   A63 - A63   2009年9月

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  • Taste Signal Transnission from Fungiform Taste Bud Cells to Chorda Tympani Nerve Fibers in Mice

    Ryusuke Yoshida, Yoshinori Murata, Toshiaki Yasuo, Keiko Yasumatsu, Noriatsu Shigemura, Yuzo Ninomiya

    CHEMICAL SENSES   34 ( 3 )   E30 - E30   2009年3月

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:OXFORD UNIV PRESS  

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  • Firing Frequency-Dependent ATP Release from Type II Taste Cells in Mice

    Yoshihiro Murata, Ryusuke Yoshida, Toshiaki Yasuo, Yuchio Yanagawa, Kunihiko Obata, Hiroshi Ueno, Robert F. Margolskee, Yuzo Ninomiya

    CHEMICAL SENSES   34 ( 2 )   J8 - J8   2009年2月

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  • Cell Types and Response Properties of Mouse Fungiform Taste Cells

    Ryusuke Yoshida, Yoshihiro Murata, Toshiaki Yasuo, Masashi Jyotaki, Yuchio Yanagawa, Kunihiko Obata, Hiroshi Ueno, Robert F. Margolskee, Yuzo Ninomiya

    CHEMICAL SENSES   34 ( 2 )   J2 - J2   2009年2月

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  • Functional analysis of T1R1/T1R3 umami taste receptor variants

    Noriatsu Shigemura, Shinya Shirosaki, Keisuke Sanematsu, Yoko Ogiwara, Misako Kawai, Ryusuke Yoshida, Yuzo Ninomiya

    NEUROSCIENCE RESEARCH   65   S176 - S176   2009年

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    DOI: 10.1016/j.neures.2009.09.934

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  • Responses of mouse fungiform taste cells to multiple bitter or sour taste compounds

    Ryusuke Yoshida, Toshiaki Yasuo, Aya Miyauchi, Yuchio Yanagawa, Kunihiko Obata, Hiroshi Ueno, Robert F. Margolskee, Yuzo Ninomiya

    NEUROSCIENCE RESEARCH   65   S175 - S175   2009年

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    DOI: 10.1016/j.neures.2009.09.926

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  • FUNCTIONAL EXPRESSION STUDY OF TAS1R1/TAS1R3 RECEPTOR VARIANTS ASSOCIATED WITH INDIVIDUAL DIFFERENCES IN HUMAN UMAMI TASTE SENSITIVITY

    Noriatsu Shigemura, Shinya Shirosaki, Keisuke Sanematsu, Yoko Ogiwara, Misako Kawai, Ryusuke Yoshida, Yuzo Ninomiya

    JOURNAL OF PHYSIOLOGICAL SCIENCES   59   488 - 488   2009年

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  • TASTE RESPONSIVENESS OF TYPE II AND III TASTE BUD CELLS IN MOUSE FUNGIFORM PAPILLAE

    Ryusuke Yoshida, Toshiaki Yasuo, Yoshihiro Murata, Masashi Jyotaki, Yuchio Yanagawa, Kunihiko Obata, Hiroshi Ueno, Sami Damak, Robert F. Margolskee, Yuzo Ninomiya

    JOURNAL OF PHYSIOLOGICAL SCIENCES   59   148 - 148   2009年

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  • Sweet sensing for regulation of food intake

    Yuzo Ninomiya, Keisuke Sanematsu, Masahumi Johtaki, Ryusuke Yoshida, Noriatsu Shigemura

    JOURNAL OF PHARMACOLOGICAL SCIENCES   109   46P - 46P   2009年

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:JAPANESE PHARMACOLOGICAL SOC  

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  • Modulation and Transmission of Sweet Taste Information for Energy Homeostasis

    Yuzo Ninomiya, Ryusuke Yoshida, Yoshihiro Murata, Keiko Yasumatsu, Tadahiro Ohkuri, Shinya Shirosaki, Keisuke Sanematsu, Toshiaki Yasuo, Yuki Nakamura, Noriatsu Shigemura

    CHEMICAL SENSES   33 ( 8 )   S23 - S23   2008年10月

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  • Firing Rate-Dependent ATP Release from Mouse Fungiform Taste Cells with Action Potentials

    Yoshihiro Murata, Ryusuke Yoshida, Toshiaki Yasuo, Yuchio Yanagawa, Kunihiko Obata, Hiroshi Ueno, Robert F. Margolskee, Yuzo Ninomiya

    CHEMICAL SENSES   33 ( 8 )   S128 - S128   2008年10月

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  • Multiple Receptor Systems for Umami Taste in Mice

    Ryusuke Yoshida, Keiko Yasumatsu, Shinya Shirosaki, Yuriko Kawato, Yoshihiro Murata, Noriatsu Shigemura, Kiyohito Nakashima, Robert F. Margolskee, Yuzo Ninomiya

    CHEMICAL SENSES   33 ( 8 )   S5 - S5   2008年10月

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:OXFORD UNIV PRESS  

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  • GFPノックインマウスを用いたII型およびIII型味細胞の応答特性の解析

    吉田竜介, 村田芳博, 安尾敏明, 上瀧将史, 安松啓子, 重村憲徳, 二ノ宮裕三

    Journal of Oral Biosciences   50 ( Supplement )   189   2008年9月

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  • II型味細胞は活動電位の頻度に依存してATPを放出する

    村田芳博, 安尾敏明, 吉田竜介, 二ノ宮裕三

    Journal of Oral Biosciences   50 ( Supplement )   189   2008年9月

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  • 単一味蕾内の複数の味細胞の応答特性

    吉田竜介, 安尾敏明, 村田芳博, 上瀧将史, 二ノ宮裕三

    日本生理学雑誌   70 ( 2 )   59   2008年2月

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    記述言語:日本語  

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  • マウス茸状乳頭味細胞の活動電位依存性ATP放出

    村田芳博, 安尾敏明, 吉田竜介, 二ノ宮裕三

    日本生理学雑誌   70 ( 2 )   60   2008年2月

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  • ATP release from mouse fungiform taste cells with action potentials

    Y. Murata, T. Yasuo, R. Yoshida, Y. Ninomiya

    CHEMICAL SENSES   33 ( 2 )   J11 - J11   2008年2月

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:OXFORD UNIV PRESS  

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  • Analysis of taste responsiveness of subsets of receptor cells in the mouse single fungiform taste bud

    R. Yoshida, T. Yasuo, Y. Murata, M. Jyotaki, Y. Ninomiya

    CHEMICAL SENSES   33 ( 2 )   J11 - J11   2008年2月

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:OXFORD UNIV PRESS  

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  • マウスII型味細胞の発火頻度依存性ATP放出

    村田芳博, 吉田竜介, 安尾敏明, 柳川右千夫, 小幡邦彦, 植野洋志, Margolskee, R.F, 二ノ宮裕三

    日本味と匂学会誌   15 ( 3 )   381 - 384   2008年

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  • ATP release from type II taste cells depending on firing rate

    Yoshihiro Murata, Ryusuke Yoshida, Toshiaki Yasuo, Yuchio Yanagawa, Kunihiko Obata, Hiroshi Ueno, Robert F. Margolskee, Yuzo Ninomiya

    NEUROSCIENCE RESEARCH   61   S178 - S178   2008年

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:ELSEVIER IRELAND LTD  

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  • Abnormal taste perception in mine lacking the Type 3 IP3 Receptor

    Chihiro Hisatsune, Keiko Yasumatsu, Hiromi Takahashi-Iwanaga, Naoko Ogawa, Yukiko Kuroda, Ryusuke Yoshida, Yuzo Ninomiya, Katsuhiko Mikoshiba

    NEUROSCIENCE RESEARCH   61   S249 - S249   2008年

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:ELSEVIER IRELAND LTD  

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  • Analysis of signal transductions for umami taste by single fiber recordings in the chorda tympani nerve of T1R3-and TRPM5-KO mice

    Keiko Yasumatsu, Ryusuke Yoshida, Robert F. Margolskee, Yuzo Ninomiya

    NEUROSCIENCE RESEARCH   61   S179 - S179   2008年

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:ELSEVIER IRELAND LTD  

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  • Different response properties among cell types of taste receptor cells

    Ryusuke Yoshida, Yoshihiro Murata, Toshiaki Yasuo, Masashi Jyotaki, Yuchio Yanagawa, Kunihiko Obata, Hiroshi Ueno, Robert F. Margolskee, Yuzo Ninomiya

    NEUROSCIENCE RESEARCH   61   S248 - S248   2008年

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:ELSEVIER IRELAND LTD  

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  • 味細胞の細胞型と応答特性

    植野 洋志, 吉田 竜介

    日本味と匂学会誌   15   285 - 288   2008年

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  • II型およびIII型味細胞の発火頻度依存性ATP放出

    村田 芳博, 吉田 竜介, 安尾 敏明, 柳川 右千夫, 小幡 邦彦, 植野 洋司, Margolskee Robert F, 二ノ宮 裕三

    日本生理学会大会発表要旨集   2008 ( 0 )   167 - 167   2008年

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    出版者・発行元:一般社団法人 日本生理学会  

    Taste signals are transmitted from taste cells to gustatory nerve fibers through chemical synapses. Taste cells are morphologically classified into four types: I, II, III and basal cells. Among them, chemical synapses are observed only in type III cells with putative sour receptors. However, sweet, bitter and umami receptors are expressed in type II cells, and the mechanisms have not been elucidated. Recent reports have highlighted the role of ATP as a key neurotransmitter. Here we tried to detect ATP release from single taste cells with action potentials in mouse fungiform papillae. The action potentials were recorded with the electrode basolaterally attached to a cell. When an increase in the firing rate was observed in response to a tastant, the electrode solution was applied for luciferase assay to determine the ATP. Type II and III cells express gustducin and glutamic acid decarboxylase (GAD67), respectively. We identified these cell types with transgenic mice expressing GFP in gustducin- or GAD67-positive cells. When Type II cells responded to saccharin or quinine, ATP was detected in a firing rate-dependent manner. When Type III cells increased the firing rate by application of HCl, ATP was below the detection limit. The results suggest that the amount of ATP released from taste cells differ with the response properties, or that type III cells release another neurotransmitter. &lt;b&gt;[J Physiol Sci. 2008;58 Suppl:S167]&lt;/b&gt;

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  • 単一味蕾中の複数の味受容細胞は様々な応答特性を持つ

    吉田竜介, 安尾敏明, 村田芳博, 安松啓子, 重村憲徳, 二ノ宮裕三

    Journal of Oral Biosciences   49 ( Supplement )   171   2007年8月

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    記述言語:日本語  

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  • マウス味細胞の味刺激応答とATP放出

    村田芳博, 安尾敏明, 吉田竜介, 二ノ宮裕三

    Journal of Oral Biosciences   49 ( Supplement )   172   2007年8月

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    記述言語:日本語  

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  • Analysis of salt taste signal transduction using salty peptides and KT-1 cells

    T. Ookura, K. Yasumatsu, Y. Ito, R. Yoshida, T. Kawai, Y. Kusakabe, Y. Shindo, A. Hino, Y. Ninomiya

    CHEMICAL SENSES   32 ( 2 )   J2 - J2   2007年2月

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:OXFORD UNIV PRESS  

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  • Relation of polymorphisms of ENaC Subunits to mouse strain differences in amiloride sensitive salt responses

    N. Shigemura, T. Ohkuri, C. Sadamitsu, K. Yasumatsu, R. Yoshida, G. K. Beauchamp, A. Bachimanov, Y. Ninomiya

    CHEMICAL SENSES   32 ( 2 )   J6 - J6   2007年2月

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:OXFORD UNIV PRESS  

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  • Response properties of NaCl responsive taste cells in mouse fungiform papillae: Amiloride-sensitive and insensitive taste cells

    R. Yoshida, T. Ohkuri, K. Yasumatsu, N. Shigemura, Y. Ninomiya

    CHEMICAL SENSES   32 ( 2 )   J6 - J6   2007年2月

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:OXFORD UNIV PRESS  

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  • Association between polymorphism of the sweet receptor gene, Tas1r3 and gurmarin sensitivity

    K. Sanematsu, K. Yasumatsu, R. Yoshida, N. Shigemura, Y. Ninomiya

    CHEMICAL SENSES   32 ( 2 )   J5 - J5   2007年2月

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:OXFORD UNIV PRESS  

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  • Temperature dependency of the chorda tympani nerve response to sweeteners in C57BL/6N and BALB/c mice

    T. Ohkuri, K. Yasumatsu, R. Yoshida, N. Shigemura, Y. Ninomiya

    CHEMICAL SENSES   32 ( 2 )   J5 - J5   2007年2月

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:OXFORD UNIV PRESS  

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  • Behavioral analysis of responses to sweet substances in T1R3-KO mice

    S. Shirosaki, R. Yoshida, N. Shigemura, K. Yasumatsu, R. F. Margolskee, Y. Ninomiya

    CHEMICAL SENSES   32 ( 2 )   J5 - J6   2007年2月

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:OXFORD UNIV PRESS  

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  • マウス茸状乳頭味細胞のATP放出

    村田芳博, 安尾敏明, 吉田竜介, 二ノ宮裕三

    日本味と匂学会誌   14 ( 3 )   391 - 394   2007年

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  • 単一細胞応答の観点からみたマウス茸状乳頭味蕾の応答性

    吉田竜介, 安尾敏明, 村田芳博, 上瀧将史, 二ノ宮裕三

    日本味と匂学会誌   14 ( 3 )   395 - 398   2007年

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  • 1P179 味刺激で誘発される活動電位に依存したマウス味細胞のATP放出(化学受容,ポスター発表,第45回日本生物物理学会年会)

    村田 芳博, 吉田 竜介, 安尾 敏明, 柳川 右千夫, 小幡 邦彦, 植野 洋司, Margolskee Robert F, 二ノ宮 裕三

    生物物理   47 ( 0 )   2007年

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    記述言語:英語   出版者・発行元:一般社団法人 日本生物物理学会  

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  • 1P180 味細胞の細胞型による応答特性の差異(化学受容,ポスター発表,第45回日本生物物理学会年会)

    吉田 竜介, 村田 芳博, 安尾 敏明, 上瀧 将史, 柳川 右千夫, 小幡 邦彦, 植野 洋司, Margolskee Robert F, 二ノ宮 裕三

    生物物理   47 ( 0 )   2007年

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    記述言語:英語   出版者・発行元:一般社団法人 日本生物物理学会  

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  • Modulations of sweet taste responses by salts, acids and bitter compounds in the mouse chorda tympani nerve

    Keiko Yasumatsu, Ryusuke Yoshida, Robert F. Margolskee, Yuzo Ninomiya

    NEUROSCIENCE RESEARCH   58   S217 - S217   2007年

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:ELSEVIER IRELAND LTD  

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  • Polymorphisms of ENaC subunits relate to mouse strain differences in amiloride sensitive salt responses

    Noriatsu Shigemura, Tadahiro Ohkuri, Chiharu Sadamitsu, Keiko Yasumatsu, Ryusuke Yoshida, Gary K. Beauchamp, Alexander A. Bachmanov, Yuzo Ninomiya

    NEUROSCIENCE RESEARCH   58   S217 - S217   2007年

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:ELSEVIER IRELAND LTD  

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  • Multiple receptors, transduction pathways and fiber types underlie umami taste in mice

    K. Yasumatsu, R. Yoshida, N. Shigemura, S. Damak, R. F. Margolskee, Y. Ninomiya

    CHEMICAL SENSES   31 ( 8 )   E88 - E89   2006年10月

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:OXFORD UNIV PRESS  

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  • Formation of taste neural coding channels

    R Yoshida, N Shigemura, K Yasumatsu, Y Ninomiya

    CHEMICAL SENSES   31 ( 1 )   J2 - J3   2006年1月

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:OXFORD UNIV PRESS  

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  • Behavioral analysis of responses to quinine in Trpm5 KO mice

    S Shirosaki, R Yoshida, N Shigemura, K Yasumatsu, RF Margolskee, Y Ninomiya

    CHEMICAL SENSES   31 ( 1 )   J12 - J12   2006年1月

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:OXFORD UNIV PRESS  

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  • NaCl induced responses of mouse fungiform taste cells: existence of amiloride sensitive and insensitive taste cells

    Ryusuke Yoshida, Tadahiro Ohkuri, Keiko Yasumatsu, Noriatsu Shigemura, Yuzo Ninomiya

    NEUROSCIENCE RESEARCH   55   S251 - S251   2006年

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:ELSEVIER IRELAND LTD  

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  • Abstracts of the 27th Annual Meeting of the Japan Neuroscience Society and the 3rd Joint Meeting of the Japan Neuroscience Society and the Japanese Society for Neurochemistry (Neuro 2004) (vol 51, pg 219, 2005)

    K Yasumatsu, N Shigemura, R Yoshida, S Damak, RF Margolskee, Y Ninomiya

    NEUROSCIENCE RESEARCH   51 ( 2 )   219 - 219   2005年2月

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    記述言語:英語   出版者・発行元:ELSEVIER SCI IRELAND LTD  

    DOI: 10.1016/j.neures.2004.12.003

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  • 食塩嗜好と味細胞応答:アンギオテンシン2による修飾

    二ノ宮 裕三, 重村 憲徳, 吉田 竜介

    助成研究報告集   2004   245 - 254   2004年

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    記述言語:日本語   出版者・発行元:ソルト・サイエンス研究財団  

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  • 味を感じる:神経メカニズム (特集1 分子を感じる:感覚の分子生物学)

    安松 啓子, 三浦 裕仁, 吉田 竜介

    細胞工学   21 ( 12 )   1429 - 1433   2002年12月

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    記述言語:日本語   出版者・発行元:秀潤社  

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    その他リンク: http://search.jamas.or.jp/link/ui/2003145795

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講演・口頭発表等

  • Signaling cascade for the sweet suppressive effect of leptin

    吉田 竜介

    The 18th ISMNTOP  2019年11月3日 

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    開催年月日: 2019年11月2日 - 2019年11月3日

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  • 体内甘味受容機構とその役割 招待

    吉田竜介

    感覚研究コンソーシアム・第 1 回味覚ワーキンググループ 「舌と味覚」  2021年5月14日 

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    会議種別:口頭発表(招待・特別)  

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  • 末梢における味覚情報処理 招待

    吉田 竜介

    第40回岡山歯学会総会・学術集会  2019年12月15日 

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  • 塩による甘味増強のメカニズム

    吉田竜介, 實松敬介

    ソルトサイエンス研究財団 平成30年度助成研究発表会  2019年7月25日 

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  • 味覚と健康 招待

    吉田 竜介

    第2回健康食品管理士会中国支部研修会  2019年1月27日 

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    記述言語:日本語   会議種別:公開講演,セミナー,チュートリアル,講習,講義等  

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  • 味細胞におけるレプチンシグナリング 招待

    吉田 竜介

    第52回味と匂学会大会  2018年10月29日 

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    記述言語:日本語   会議種別:口頭発表(招待・特別)  

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  • 末梢における甘味の受容と調節メカニズム 招待

    吉田 竜介

    第60回歯科基礎医学会学術大会  2018年9月6日 

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    記述言語:日本語   会議種別:口頭発表(招待・特別)  

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  • From Kyushu to Okayama: My research history 招待

    吉田 竜介

    Kyudai Oral Bioscience & OBT Research Center Joint International Symposium 2019  2018年3月2日 

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受賞

  • 歯科基礎医学会賞生理学部門

    2011年11月   歯科基礎医学会  

    吉田 竜介

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  • 研究奨励賞

    2010年9月   日本味と匂学会  

    吉田 竜介

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  • 優秀ポスター発表賞生理学部門

    2005年9月   歯科基礎医学会  

    吉田 竜介

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共同研究・競争的資金等の研究

  • 栄養素特異的な味細胞-味神経可塑的マッチング機構の解明

    研究課題/領域番号:18K19652  2018年06月 - 2021年03月

    日本学術振興会  科学研究費助成事業 挑戦的研究(萌芽)  挑戦的研究(萌芽)

    重村 憲徳, 吉田 竜介, 實松 敬介, 高井 信吾

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    配分額:6370000円 ( 直接経費:4900000円 、 間接経費:1470000円 )

    近年、「味覚受容体」は、口腔のみならず視床下部や消化管、膵臓β細胞など様々な栄養関連臓器で発現することから、味覚の異常は、口腔のみならず、“全身の臓器でも味覚異常”が生じて、栄養・摂食・嚥下障害や生活習慣病(高血圧・糖尿病・高脂血症)の発症原因となる可能性が示唆されている。
    味細胞は少なくとも5種類に分類され、それぞれ異なる5基本味に対する特異的な味覚受容体を発現して味物質を受容している。また、この味細胞の寿命は約10日と短いにも関わらず、味覚情報(認知)は恒常的に維持されている。これらのことから、味細胞と味神経とは、生まれてから死ぬまでの全ライフコースを通して絶えず配線/断線を繰り返しながら味質選択的に配線されることで、外・内環境に適切な「摂食行動適応」が達成される可能性が示唆される。その一方で、加齢や不規則な生活習慣により 「ミス配線」も起こりやすくなることも考えられ、この慢性化が上記の疾病発症、つまり、「口腔および全身の味覚感受性の低下」から「体内栄養素の代謝異常」、そして「生活習慣病など個体機能の低下」へと繋がる可能性が推定された。
    そこで、本研究では、この“未知の動的な配線制御機構”を明らかにするために、我々の予備実験から見出された“味蕾”および“味神経”に「共通」に発現する16種類の細胞表面蛋白(Cadherin: Cdh)ファミリーに着目し、これらが5基本味(=5栄養素)(甘味=糖、塩味=Na+、うま味=アミノ酸、酸味=H+、苦味=毒物)に特異的な配線制御分子として機能している可能性について遺伝子改変マウス/分子生物/神経生理/行動生理学的解析により追求する。

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  • 味細胞オミクス新技術の開発:高カロリーセンシングとシグナル伝達分子ロジックの探求

    研究課題/領域番号:18K19653  2018年06月 - 2020年03月

    日本学術振興会  科学研究費助成事業 挑戦的研究(萌芽)  挑戦的研究(萌芽)

    二ノ宮 裕三, 吉田 竜介, 安松 啓子

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    配分額:6240000円 ( 直接経費:4800000円 、 間接経費:1440000円 )

    本研究は、マウス単一味細胞網羅的遺伝子解析を基に脂質味と高カロリー味受容関連分子群を予測し、それらの味細胞における発現と味細胞・味神経・行動応答を検索し、分子機能解析を行った。その結果、既知の5基本味(甘・酸・塩・苦・うま味)情報経路以外に、GPR120など受容体分子を介する脂質味特異的経路や、脂質・糖など各種輸送体や受容体、代謝センサーKATPチャネルなど分子群が共存するカロリー味受容細胞や嗜好性味情報神経経路が存在することが示唆された。すなわち、味細胞遺伝子解析と味応答解析を融合させた味細胞オミクス新技術は、新知見を導き、その有効性が示唆された。

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  • 味細胞甘味調節機構の分子・生理基盤の解明

    研究課題/領域番号:18K09507  2018年04月 - 2021年03月

    日本学術振興会  科学研究費助成事業 基盤研究(C)  基盤研究(C)

    吉田 竜介

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    配分額:4290000円 ( 直接経費:3300000円 、 間接経費:990000円 )

    本研究は、レプチンや内因性カンナビノイドにより甘味受容細胞で活性化される細胞内情報伝達経路を焙り出すとともに、その細胞特異性についても追及し、甘味感受性調節機構の分子・生理基盤を明らかとすることを目的とする。
    本年度は、前年度に引き続き、甘味受容細胞でのレプチンのシグナル経路について検討した。甘味受容体コンポーネントT1R3を発現する細胞を同定できる遺伝子改変マウス(T1R3-GFPマウス)を用い、GFP発現味細胞のショ糖応答に対するレプチン投与の効果を調べると、約30%程度の応答抑制効果が見られ、これは、PI3キナーゼ(PI3K)阻害剤(wortmannin、LY294002)により阻害された。一方、STAT3阻害薬(Stattic)、SHP2阻害薬(SHP099)はレプチンの甘味抑制効果には影響を与えなかった。前年度、および今年の結果から、レプチンは甘味細胞においてPIK3を活性化することで甘味抑制効果を発揮すると考えられる。また、レプチンの最終ターゲットとなるKATPチャネルの味覚への関与をin vivoで調べるため、KATPチャネル開口剤であるDiazoxide投与のマウス短時間リック応答への影響について解析した。マウスに100mMショ糖に対し嫌悪条件づけを施し、各種味溶液へのリック応答を調べると、Diazoxide投与およびレプチン投与により各種甘味物質に対するリック応答が増加した。これは甘味に対する感受性がレプチン投与およびDiazoxide投与により減少することを示す。レプチン投与とDiazoxide投与の間で甘味抑制効果は変わらなかったことから、レプチンはin vivoにおいても甘味味細胞のKATPチャネルを開口することにより甘味抑制効果を発揮することが示唆される。

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  • 口腔脳腸・味情報-内分泌連関食調節系の酸化ストレスによる変調と修復の分子生理基盤

    研究課題/領域番号:18H02968  2018年04月 - 2021年03月

    日本学術振興会  科学研究費助成事業 基盤研究(B)  基盤研究(B)

    二ノ宮 裕三, 吉田 竜介, 岩田 周介, 安松 啓子

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    配分額:17290000円 ( 直接経費:13300000円 、 間接経費:3990000円 )

    口腔・腸の甘味・塩味受容機構は、体に必要な栄養素の検知や吸収に働くが、その感度は脳の食欲調節因子レプチン・カンナビノイド・アンギオテンシンIIによる最適化制御を受け、生体恒常性の維持に寄与している。高脂肪高甘味食などの過剰摂取は、この味調節系に変調をもたらし肥満に導くことも知られている。また、上記味調節因子は酸化ストレス関連因子としても知られ、酸化により標的分子内SH基を修飾し(S-グルタチオン化:SSG化)、機能変化による調節効果の自己抑制的な低下を導く可能性が示唆される。本研究は、それら酸化ストレス下でSSG化される標的分子による変調と回復の動作原理を明らかにするため、課題1: 酸化ストレスによる味調節系の変調と修復の機序について、調節因子の標的チャネル分子である代謝センサー(KATP:甘味)、温度センサー(TRPV4:甘味)、Naセンサー(ENaC:塩味)について、甘味・塩味受容細胞の興奮性のSSG化による変調と還元剤による修復を細胞分子生理学的に解析し、課題2: 酸化ストレス関連分子・遺伝子群の味細胞における発現と機能を検索する。
    昨年度、課題1では、T1R3欠損マウスを用いた味応答解析により、酸化ストレス誘導剤により、糖輸送体SGLTs-KATPチャネル経由の甘味応答が増強されるが、還元剤によりその効果が消失すること、また、野生型マウスを用いた追加実験により、甘味の温度増強がTRPV4の阻害剤で部分的に低下すること、ENaCs阻害剤アミノライドで抑制される塩味応答成分が、酸化ストレス誘導剤で低下し、還元剤で回復することが明確になった。課題2では、RT-PCR解析で、酸化ストレス分子標的の経路上にある酸化還元に関与する各種酵素や輸送体など分子の発現が、BioGeeを用いた解析では、酸化ストレス変化が味細胞I型に最も強く現れることが示唆された。

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  • 口腔脳腸・味情報‐内分泌連関の形成原理と分子基盤の解明

    研究課題/領域番号:15H02571  2015年04月 - 2018年03月

    日本学術振興会  科学研究費助成事業 基盤研究(A)  基盤研究(A)

    二ノ宮 裕三, 重村 憲徳, 吉田 竜介, 實松 敬介, 岩槻 健, 安松 啓子, 高井 信吾

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    配分額:40820000円 ( 直接経費:31400000円 、 間接経費:9420000円 )

    本研究は、口腔・脳・腸で協調して働く味情報・内分泌連関系の分子基盤と食調節機能について検索した。その結果、マウス味細胞・腸内分泌細胞はノンカロリー物も受容する甘味受容体T1R2/T1R3と糖特異的輸送体経路を共にもち、脳の食欲抑制ホルモン・レプチンは糖輸送体経路上の代謝センサーKATPチャネルに働き、細胞興奮性を低下させ甘味応答や糖吸収能を抑制することがわかった。また、腸管ホルモンのCCKは、味細胞では苦味の神経情報伝達に寄与することが判明した。高脂肪食摂取によるレプチン濃度の上昇は、代謝センサーを介するエネルギー調節能を低下させ、肥満の危険性を増加させることが示唆された。

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  • 味細胞における苦味情報のコーディング

    研究課題/領域番号:26462815  2014年04月 - 2017年03月

    日本学術振興会  科学研究費助成事業 基盤研究(C)  基盤研究(C)

    吉田 竜介

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    配分額:4810000円 ( 直接経費:3700000円 、 間接経費:1110000円 )

    本研究では、①様々な苦味物質に対する応答プロファイルによりマウス苦味受容細胞が幾つかのタイプに分類されること、②茸状、有郭乳頭間でこれら苦味細胞の応答プロファイルに差がないこと、③これら細胞での苦味受容にはgustducin-PLCβ2-TRPM5を介する伝達経路が重要であること、④ヒト苦味受容体阻害剤がマウスの苦味応答には影響を与えないこと、⑤CCKが苦味受容細胞から味神経線維への情報伝達に関与する可能性を示した。これらにより、味細胞における苦味受容機構について明らかとし、末梢における苦味情報の伝達及びコーディングについての知見を得た。

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  • 脂質高嗜好性形成のシグナル受容・調節・伝達の分子神経機構の解明

    研究課題/領域番号:26670810  2014年04月 - 2016年03月

    日本学術振興会  科学研究費助成事業 挑戦的萌芽研究  挑戦的萌芽研究

    二ノ宮 裕三, 重村 憲徳, 吉田 竜介

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    配分額:3510000円 ( 直接経費:2700000円 、 間接経費:810000円 )

    本研究は、脂質嗜好形成に関わるシグナル受容・調節・伝達の分子神経機構を検索した。
    マウスには脂質選択的な情報を伝える神経情報経路が存在した。甘味/うま味/Ca味ベスト神経線維の一部は脂肪酸感受性も示した。高脂肪食摂取肥満マウスは、肥満に伴い、食欲抑制に働くレプチンの血中濃度が上昇し、甘味抑制効果が低下した。逆に食欲増強に働くエンドカンナビノイド(eCB)の甘味増強効果が現れた。また、糖・脂肪酸混合液の繰り返し刺激は応答を漸増させた。この増強はeCB受容体阻害で消失し、eCBを介して起こることが示唆された。この脂肪酸の糖応答の増強は、肥満への移行過程にも関与する可能性が考えられる。

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  • 味蕾内GABA系を介した味細胞の機能的成熟

    研究課題/領域番号:23689076  2011年04月 - 2014年03月

    日本学術振興会  科学研究費助成事業 若手研究(A)  若手研究(A)

    吉田 竜介

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    配分額:23530000円 ( 直接経費:18100000円 、 間接経費:5430000円 )

    本研究では、①末梢の味覚受容器官である味蕾の形態的な発生・発達やその神経支配の過程において味蕾内のGABAは明確な役割を持たない可能性、②味蕾内でGABAは一部味細胞の興奮により放出されること、③味細胞の細胞内Cl-濃度は非常に高く、GABAにより興奮性の応答が生じることを示し、味蕾内ではGABAは主に味覚受容の調節機構の一旦として機能する可能性が示唆された。

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  • 遺伝子改変マウスを用いた味細胞の甘味受容・感受性調節機構の解析

    研究課題/領域番号:21791808  2009年 - 2010年

    日本学術振興会  科学研究費助成事業 若手研究(B)  若手研究(B)

    吉田 竜介

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    配分額:4160000円 ( 直接経費:3200000円 、 間接経費:960000円 )

    本研究では、(1)内因性カンナビノイドが甘味受容細胞の応答を増強することおよび、その増強効果は味細胞に発現するCB1受容体を介し生じること、(2)甘味受容体であるT1R3を発現する細胞は甘味、うま味刺激に対し応答を示すこと、(3)甘味、うま味の受容・情報伝達に関する遺伝子(T1R3、gustducin、TRPM5)を欠損した遺伝子改変マウスにおいて、T1R3発現細胞が味刺激に対して応答を示さないこと、(4)T1R3発現細胞にはgustducin以外にもGαサブユニット(11、14、s、q、i2)が存在することを明らかとした。

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  • 味細胞による味覚情報のディスクリミネーション

    研究課題/領域番号:19791367  2007年 - 2008年

    日本学術振興会  科学研究費助成事業 若手研究(B)  若手研究(B)

    吉田 竜介

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    配分額:3680000円 ( 直接経費:3200000円 、 間接経費:480000円 )

    本研究では、(1)5基本味(甘・苦・塩・酸・うま味)のうち、甘味、苦味、うま味を受容する味細胞と酸味を受容する味細胞の細胞型が異なること、
    (2)塩味受容細胞はアミロライド感受性により2つのタイプが存在すること、
    (3)うま味の受容細胞には甘味とうま味を受容する味細胞、うま味特異的味細胞が存在し、それぞれにうま味相乗効果の有無により更に2つのタイプに分類されることを明らかにした。これらは味情報が味細胞レベルで分別されている可能性を示唆する。

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  • 味覚センサーの空間的、時間的、種間的モーダルシフトによる細胞応答、個体応答の変化

    研究課題/領域番号:18077004  2006年 - 2010年

    日本学術振興会  科学研究費助成事業 特定領域研究  特定領域研究

    二ノ宮 裕三, 重村 憲徳, 吉田 竜介

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    配分額:64400000円 ( 直接経費:64400000円 )

    味覚セルセンサーのモーダルシフトによる細胞応答・個体応答の変化を検索し、甘味センサーは食欲調節物質のレプチンとエンドカンナビノイドによって相互拮抗的な感度調節を受けること、マウスの甘味抑制ペプチド(ヒトに無効)・グルマリンはその甘味受容体T1r3の細胞外ドメイン(一部T1r2)に働くこと、塩味センサーはENaCチャネルの3種のサブユニットの内、αサブユニットのアミノ酸変異がモーダルシフトをもたらすことが判明した。

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  • 食の調節機構としての味覚の受容・認知機序の解明:味覚健康科学の創成

    研究課題/領域番号:18109013  2006年 - 2010年

    日本学術振興会  科学研究費助成事業 基盤研究(S)  基盤研究(S)

    二ノ宮 裕三, 重村 憲徳, 吉田 竜介, 實松 敬介

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    配分額:112450000円 ( 直接経費:86500000円 、 間接経費:25950000円 )

    本研究は、味の受容・感受性調節とその食調節における役割を検索した。その結果、甘味が特定の味細胞で受容・細胞内伝達され、アデノシン3リン酸を介して、神経伝達されること、その感度は血中レプチン濃度と負の相関を示し、概日リズムが同調するが、肥満者はそれが消失すること、さらに、ヒト遺伝子多型解析からうま味受容体が複数存在することを示し、味の受容・情報伝達の新知見と、肥満との連関など味覚の新機能を見出した。

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  • 味細胞の生理機能と発現分子との連関:シングルセルRT-PCR法による解析

    研究課題/領域番号:17791325  2005年 - 2006年

    日本学術振興会  科学研究費助成事業 若手研究(B)  若手研究(B)

    吉田 竜介

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    配分額:3300000円 ( 直接経費:3300000円 )

    本研究は、マウスの舌上皮・味蕾標本を用いることにより味覚受容器の構築を大きく損なうことなく細胞の生存性を高め、ルーズパッチ法により味細胞の味刺激に対する応答を記録し、その細胞における発現遺伝子をマルチプレックス・シングルセルRT-PCR法により検索することにより、受容体などの味覚関連分子の味細胞での発現と味細胞の応答特性との関連を解析することを目的とする。
    マウス茸状乳頭味細胞のNaCl応答をルーズパッチ法で解析した結果、およそ半数の細胞が上皮性ナトリウムチャネル(ENaC)の阻害剤であるアミロライドに感受性があり(AS細胞)、残り半数はアミロライドに感受性を示さなかった(Al細胞)。AS細胞はNaClに特異的な応答を示し、Al細胞はNaCl以外にも電解質溶液(KCI、HCIなど)に応答を示した。アミロライドの効果は味孔側に与えられた場合に限られ、基底外側膜側に与えた場合には効果がなかった。これらの味細胞の応答特性や存在比は、鼓索神経にみられる2つのタイプ(アミロライド感受性のNタイプと非感受性のEタイプ)の線維のそれらと一致することが示唆された。シングルセルRT-PCRにより、これらの細胞でのENaCの発現を調べたところ、AS細胞ではα-ENaCの発現が検出され、Al細胞ではENaCサブユニットの発現は検出できなかったことから、AS細胞ではENaCがNaCl応答に関与している可能性が示唆される。
    また、味細胞のグルタミン酸(MSG)応答を解析した結果、MSG応答細胞はサッカリンに応答する細胞、NaClに応答する細胞、MSGのみに応答する細胞に大別された。これらの応答特性の違いと、発現遺伝子との関連性については、現在の所、まだ明らかにはできていない。

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担当授業科目

  • 人体生理学 (2021年度) 集中  - その他

  • 動物的機能の生理学 (2021年度) 第1学期  - 水1,水2,水3

  • 口腔機能再建学演習 (2021年度) 特別  - その他

  • 口腔生理学 (2021年度) 第3学期  - 水1~3,木4

  • 口腔生理学実習 (2021年度) 第3学期  - 木5,木6,木7

  • 口腔生理学I(演習・実習) (2021年度) 特別  - その他

  • 口腔生理学I(講義・演習) (2021年度) 特別  - その他

  • 口腔生理学II(演習・実習) (2021年度) 特別  - その他

  • 口腔生理学II(講義・演習) (2021年度) 特別  - その他

  • 植物的機能の生理学 (2021年度) 第2学期  - 水1,水2,水3

  • 総合歯科医学1 (2021年度) 第1学期  - 火1,火2,火3

  • 総合歯科医学2 (2021年度) 第2学期  - 月3,火3,水3,金1~2

  • 動物的機能の生理学 (2020年度) 第1学期  - 水1,水2,水3

  • 口腔機能再建学演習 (2020年度) 通年  - その他

  • 口腔機能再建学総論 (2020年度) 通年  - その他

  • 口腔生理学 (2020年度) 第3学期  - 水1~3,木4

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  • 口腔生理学I(講義・演習) (2020年度) 特別  - その他

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社会貢献活動

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    津山高等学校  2019年6月21日

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    うま味研究会  うま味研究会 公開シンポジウム  2019年6月7日

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  • 味覚の不思議 ~口だけではないその機能~

    役割:講師

    岡山大学研究推進機構  第72回岡大サイエンスカフェ  2019年5月16日

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