| Project/Area Number |
23500469
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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 | Keio University |
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Principal Investigator |
MATSUDA Keiko 慶應義塾大学, 医学部, 助教 (40383765)
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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 |
¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2013: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2012: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2011: ¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
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| Keywords | シナプス形成 / シナプス可塑性 / 神経栄養因子 / シナプス / 海馬 / 神経科学 / 脳・神経 / 神経細胞 / 可塑性 |
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| Research Abstract |
We had proposed a new molecular mechanism underlying cerebellar parallel fiber synapse formation; secreted Cbln1 links its two receptors, GluD2 and Neurexin, across synaptic cleft, leading bidirectional synaptic differentiation. In hippocampal CA1 pyramidal neurons, most related receptor, GluD1 is restrictedly localized in TA layer which is the most distal part in CA1 dendrites, where GluD1 is responsible for establishment of LTD. Analysis in Cbln1 or Cbln4 knockout mice, restricted localization of GluD1 in TA layer requires its ligands Cbln1 and Cbln4.
Thus we now propose the more general function of protein complex, Neurexin-Cbln-GluD in synapse formation and establishment of neuronal circuit precisely, not only in cerebellum but also in hippocampus.
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