Regulation of synaptic plasticity and learning by cross-talk of G protein-coupled receptors
Project/Area Number |
20500284
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Neuroscience in general
|
Research Institution | University of Toyama |
Principal Investigator |
TABATA Toshihide University of Toyama, 大学院・理工学研究部(工学), 准教授 (80303270)
|
Project Period (FY) |
2008 – 2010
|
Project Status |
Completed (Fiscal Year 2010)
|
Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2010: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2009: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2008: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
|
Keywords | 神経科学 / 生理学 / 脳・神経 / シグナル伝達 / シナプス可塑性 / 学習 / 記憶 / 運動 |
Research Abstract |
Our electrophysiological analyses in cultured mouse cerebellar Purkinje cells suggest that ligand-activated adenosine A1 receptor (A1R) impedes cerebellar long-term depression (LTD) by decreasing the glutamate-sensitivity of type-1 metabotropic glutamate receptor (mGluR1), a key trigger of induction of cerebellar LTD. Our in-vivo behavioral analyses showed that activation of B-type gamma-amino butyric acid receptor (GABAbR) facilitated cerebellar LTD-dependent motor learning. These findings suggest that in response to neuromodulators in the cereberospinal fluid, A1R and GABAbR modulate mGluR1 and thereby regulate induction of synaptic plasticity and learning.
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Report
(4 results)
Research Products
(46 results)