| Project/Area Number |
23500384
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Neuroscience in general
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| Research Institution | University of Toyama |
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Principal Investigator |
TABATA Toshihide 富山大学, 大学院理工学研究部(工学), 准教授 (80303270)
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| Co-Investigator(Renkei-kenkyūsha) |
KAMIKUBO Yuji 順天堂大学, 医学部, 助教 (80509670)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2012: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2011: ¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
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| Keywords | Ｇタンパク質 / シナプス可塑性 / ニューロン / 受容体 / 学習 / 小脳 / 生理学 / 神経科学 / Gタンパク質 |
|---|
| Research Abstract |
In cerebellar Purkinje cells, B-type gamma-aminobutyric acid receptor (GABAbR) and type-1 adenosine receptor (A1R) are suggested to modulate type-1 metabotropic glutamate receptor (mGluR1) whose intracellular signaling triggers induction of cerebellar long-term depression (LTD). Using a machine vision-based optokinetic reflex (OKR) measuring system, we found that in mice, cerebellar injection of a GABAbR agonist facilitated OKR adaptation, a cerebellar LTD-dependent learning. Moreover, using in-vitro preparations, we found that A1R interacted with mGluR1 via its C-terminus and that A1R activation suppressed the LTD of Purkinje cell's glutamate-responsiveness by lowering mGluR1's ligand-sensitivity in a G protein-independent manner. The hetero-G protein-coupled receptor interplay may influence central synaptic plasticity and learning.
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