| Project/Area Number |
26430079
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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 |
Neurochemistry/Neuropharmacology
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| Research Institution | National Institute for Physiological Sciences |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
深澤 有吾 福井大学, 学術研究院医学系部門, 教授 (60343745)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2016: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | 小脳 / 顆粒細胞 / 分子層介在ニューロン / 興奮性シナプス後電流 / スライスパッチクランプ法 / グルタミン酸輸送体 / 電位依存性カルシウムチャネル |
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| Outline of Final Research Achievements |
Paired pulse activation of rat cerebellar granule cell (GC) ascending axons at short intervals (30-100 ms) causes not only increase in the peak amplitude (PPFamp) of the second EPSC (EPSC2) recorded from molecular layer interneurons (MLIs) but also prolongation of the EPSC2 decay time (PPPdecay) relative to those of the first EPSC. PPFamp is resulted from transient increases in release probability (Pr) and multivesicular release (MVR), whereas PPPdecay is elicited by an increase in MVR and the subsequent pooling of MVR-glutamate among adjacent synapses. Recently, we found that PPPdecay plays a major role in Gi/o-coupled receptor-mediated presynaptic depression in the GC-MLI synapse. In this study, we focused on molecular mechanisms underlying the presynaptic depression. Dynamic modulation of presynaptic MVR and postsynaptic current decay will provide additional complexity in neuronal encoding, processing, and plasticity at the single synapse to reflect circumstances of adjacent cells.
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