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2017 Fiscal Year Final Research Report

Mechanisms for AMPA-type glutamate receptor anchoring at the synapse

Research Project

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Project/Area Number 15H04279
Research Category

Grant-in-Aid for Scientific Research (B)

Allocation TypeSingle-year Grants
Section一般
Research Field Neurochemistry/Neuropharmacology
Research InstitutionNational Institute for Physiological Sciences

Principal Investigator

FUKATA Yuko  生理学研究所, 分子細胞生理研究領域, 准教授 (40416186)

Research Collaborator YOKOI Norihiko  生理学研究所, 分子細胞生理研究領域, 助教 (50710969)
HIRATA Tetsuya  生理学研究所, 分子細胞生理研究領域, 特任助教 (90780651)
TAKAHASHI Naoki  
INAHASHI Hiroki  
SEKIYA Atsushi  
MURAKAMI Tatsuro  
FURUKAWA Sachiko  
SUZUKI Yumi  
Project Period (FY) 2015-04-01 – 2018-03-31
Keywordsシナプス / AMPA受容体 / グルタミン酸受容体 / パルミトイル化脂質修飾 / PSD-95 / てんかん / 脱パルミトイル化 / ナノドメイン
Outline of Final Research Achievements

AMPA-type glutamate receptor (AMPAR) mediates most of fast synaptic transmission in the brain. Although AMPAR dynamically enters and exits the postsynaptic membrane in a synaptic activity-dependent manner, the underlying molecular mechanism is still incompletely understood. In this study, we focused on palmitoylation and protein-protein interactions of PSD-95, an essential scaffolding protein for AMPAR. We discovered a novel enzyme, ABHD17, which catalyzes PSD-95 depalmitoylation and thereby plays an important role in the (re)organization of the postsynaptic platform for AMPAR anchoring. We also found that the epilepsy-related ligand/receptor complex of LGI1 and ADAM22 regulates AMPAR functions through the direct interaction with PSD-95. Furthermore, we revealed the structural basis of the LGI1-ADAM22 protein complex at the synapse and its patho-physiological role in epileptogenesis.

Free Research Field

神経科学、細胞生物学、生化学

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Published: 2019-03-29  

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