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Neuronal protease-activated receptor 1 drives synaptic retrograde signaling mediated by the endocannabinoid 2-arachidonoylglycerol
https://doi.org/10.24517/00013443
https://doi.org/10.24517/0001344381db5891-5b25-430a-ab16-6984f520094f
名前 / ファイル | ライセンス | アクション |
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ME-PR-SHOSAKU-M-3104.pdf (1.5 MB)
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Item type | 学術雑誌論文 / Journal Article(1) | |||||
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公開日 | 2017-10-03 | |||||
タイトル | ||||||
タイトル | Neuronal protease-activated receptor 1 drives synaptic retrograde signaling mediated by the endocannabinoid 2-arachidonoylglycerol | |||||
言語 | ||||||
言語 | eng | |||||
資源タイプ | ||||||
資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
資源タイプ | journal article | |||||
ID登録 | ||||||
ID登録 | 10.24517/00013443 | |||||
ID登録タイプ | JaLC | |||||
著者 |
Hashimotodani, Yuki
× Hashimotodani, Yuki× Ohno-Shosaku, Takako× Yamazaki, Maya× Sakimura, Kenji× Kano, Masanobu |
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著者別表示 |
少作, 隆子
× 少作, 隆子× 狩野, 方伸 |
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提供者所属 | ||||||
内容記述タイプ | Other | |||||
内容記述 | 金沢大学医薬保健研究域保健学系 | |||||
書誌情報 |
Journal of Neuroscience 巻 31, 号 8, p. 3104-3109, 発行日 2011-02-23 |
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ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 0270-6474 | |||||
ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 1529-2401 | |||||
NCID | ||||||
収録物識別子タイプ | NCID | |||||
収録物識別子 | AA10620404 | |||||
DOI | ||||||
関連タイプ | isVersionOf | |||||
識別子タイプ | DOI | |||||
関連識別子 | 10.1523/JNEUROSCI.6000-10.2011 | |||||
出版者 | ||||||
出版者 | Society for Neuroscience | |||||
抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | Protease-activated receptor 1 (PAR1) is a member of the G-protein coupled receptors that are proteolytically activated by serine proteases. Recent studies suggest a definite contribution of PAR1 to brain functions, including learning and memory. However, cellular mechanisms by which PAR1 activation influences neuronal activity are not well understood. Here we show that PAR1 activation drives retrograde endocannabinoid signaling and thereby regulates synaptic transmission. In cultured hippocampal neurons from rat, PAR1 activation by thrombin or PAR1-specific peptide agonists transiently suppressed inhibitory transmission at cannabinoid-sensitive, but not cannabinoid-insensitive, synapses. The PAR1-induced suppression of synaptic transmission was accompanied by an increase in paired-pulse ratio, and was blocked by a cannabinoid CB1 receptor antagonist. The PAR1-induced suppression was blocked by pharmacological inhibition of postsynaptic diacylglycerol lipase (DGL), a key enzyme for biosynthesis of the major endocannabinoid 2-arachidonoylglycerol (2-AG), and was absent in knock-out mice lacking the α isoform of DGL. The PAR1-induced IPSC suppression remained intact under the blockade of metabotropic glutamate receptors and was largely resistant to the treatment that blocked Ca2+ elevation in glial cells following PAR1 activation, which excludes the major contribution of glial PAR1 in IPSC suppression. We conclude that activation of neuronal PAR1 triggers retrograde signaling mediated by 2-AG, which activates presynaptic CB1 receptors and suppresses transmitter release at hippocampal inhibitory synapses. | |||||
内容記述 | ||||||
内容記述タイプ | Other | |||||
内容記述 | This work wassupported by Grants-in-Aid for Scientific Research (21220006 and 21650094 to M.K., 18-08582 to Y.H., and 20021014 and 20500357 to T.O.S.), the Strategic Research Program for Brain Sciences (Development of Biomarker Candidates for Social Behavior), and Global COE program (Integrative Life Science Based on the Study of Biosignaling Mechanisms) from Ministry of Education, Culture, Sports, Science, and Technology,Japan.Wethank A. Koseki for technical assistance, and H. Mizoguchi and K. Yamada for the generous gift of PAR1 knock-out mice. |
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権利 | ||||||
権利情報 | Copyright © Society for Neuroscience | |||||
著者版フラグ | ||||||
出版タイプ | AM | |||||
出版タイプResource | http://purl.org/coar/version/c_ab4af688f83e57aa | |||||
関連URI | ||||||
識別子タイプ | URI | |||||
関連識別子 | https://www.jneurosci.org/content/31/8/3104 | |||||
関連名称 | https://www.jneurosci.org/content/31/8/3104 | |||||
関連URI | ||||||
識別子タイプ | URI | |||||
関連識別子 | http://www.jneurosci.org/ | |||||
関連名称 | http://www.jneurosci.org/ |