2015 Fiscal Year Final Research Report
Molecular mechanisms underlying AMPA receptor trafficking during synaptic plasticity
Project/Area Number |
23240053
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Research Category |
Grant-in-Aid for Scientific Research (A)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Neurophysiology and muscle physiology
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Research Institution | Keio University |
Principal Investigator |
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Co-Investigator(Kenkyū-buntansha) |
KOHDA KAZUHISA 慶應義塾大学, 医学部, 准教授 (40334388)
KAKEGAWA WATARU 慶應義塾大学, 医学部, 専任講師 (70383718)
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Project Period (FY) |
2011-04-01 – 2016-03-31
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Keywords | グルタミン酸受容体 / エンドサイトーシス / 小脳 / シナプス可塑性 / プルキンエ細胞 / LTD / AMPA受容体 / マウス |
Outline of Final Research Achievements |
It is believed that long-term depression (LTD) is mediated by AMPA receptor endocytosis at the postsynaptic site. During LTD, AMPA receptors are first liberated from their anchoring proteins at the postsynaptic site, diffuse to the perisynaptic site, where endocytosis takes place. However how AMPA receptors are selectively endocytosed remained largely unclear. In addition, it has been a mystery why the delta2 glutamate receptor (GluD2) is crucial for induction of cerebellar LTD. In this study, we found that GluD2 determined whether anchoring proteins were dissociated from AMPA receptors. In addition, we found how clathrin adaptor protein AP-2, an essential molecule for clathrin-dependent endocytosis, accumulated at the perisynaptic site and recognized the AMPA receptor complex during LTD.
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Free Research Field |
神経生物学
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