| Project/Area Number |
23500461
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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 |
Neurophysiology and muscle physiology
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| Research Institution | Gunma University |
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Principal Investigator |
YASUDA Hiroki 群馬大学, 医学(系)研究科(研究院), 准教授 (60294071)
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| Co-Investigator(Renkei-kenkyūsha) |
MUKAI Hideyuki 神戸大学, 大学院医学研究科, 准教授 (80252758)
KOJIMA Nobuhiko 東洋大学, 生命科学部, 教授 (80215251)
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| Project Period (FY) |
2011-04-28 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2011: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | protein kinase N / 代謝型グルタミン酸受容体 / グルタミン酸トランスポーター / シナプス可塑性 / ストレス / 海馬 / PKN1 / メタ可塑性 / 神経発達 / PKN / 海馬歯状回 / 顆粒細胞 |
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| Outline of Final Research Achievements |
I investigated the roles of protein kinase N1 (PKN1) using PKN1a knockout mice and found that PKN1 activates neuronal glutamate transporter (EAAT3), reduces synaptic and extracellular glutamate, and normalizes metabotropic glutamate receptor (mGluR) function. PKN1 suppresses unnecessary mGluR5-dependent long-term depression (LTD) of glutamate synaptic transmission in the developing hippocampus. Stress ihibited EAAT3 presumably through reducing PKN1 activity and elevates neuronal excitability. So elevating PKN1 activity could activate EAAT3 and reduce epileptic neuronal activity.
I also found that priming of glutamate synaptic transmission by prior acitivity was induced in wild-type mice but that the priming was not induced in PKN1a KO mice, suggesting that PKN1 is needed in priming of excitatory synaptic transmission.
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