2008 Fiscal Year Final Research Report
Elucidation of the mechanisms and physiological significance of endocannabinoid-mediated retrograde synaptic modulation
| Project/Area Number |
17100004
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| Research Category |
Grant-in-Aid for Scientific Research (S)
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| Allocation Type | Single-year Grants |
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| Research Field |
Neuroscience in general
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| Research Institution | The University of Tokyo (2007-2009)
Osaka University (2005-2006) |
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Principal Investigator |
KANO Masanobu The University of Tokyo, 大学院・医学系研究科, 教授 (40185963)
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| Co-Investigator(Kenkyū-buntansha) |
SAKIMURA Kenji 新潟大学, 脳研究所, 教授 (40162325)
SHOSAKU Takako 金沢大学, 保健学系, 教授 (60179025)
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| Project Period (FY) |
2005 – 2008
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| Keywords | 分子 / 細胞神経科学 / ニューロン / シナプス / 神経回路 / 神経発生 / 神経発達 / 神経再生 / 神経再建 / 姿勢 / 運動制御 |
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| Research Abstract |
Endogenous cannabinoids (endocannabinoids) are released from neurons in the central nervous system in activity-dependent manners. The released endocannabinoids act retrogradely onto CB_1 cannabinoid receptors on presynaptic terminals, and suppress neurotransmitter release. This study aimed at elucidating the molecular and cellular mechanisms of endocannabinoid release from central neurons and the roles of the endocannabinoid system in brain functions. We have found that the endocannbinoid release is triggered by strong depolarization of postsynaptic neurons and the resultant elevation of Ca^<2+> concentration (Ca^<2+>-driven endocannabinoid release [ER]), strong activation of G_<q/11>-coupled receptors at basal intracellular Ca^<2+> level (basal receptor-driven endocannabinoid release [RER]), or simultaneous Ca^<2+> elevation and G_<q/11>-coupled receptor activation (Ca^<2+>-assisted RER). We have also disclosed that endocannabinoid signaling is required for motor learning in the cerebellum. Through the four years' research, we have achieved most of the original purposes.
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Research Products
(46 results)
