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2014 Fiscal Year Final Research Report

Functional difference between syntaxin1 isoforms in synaptic transmission

Research Project

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Project/Area Number 24300142
Research Category

Grant-in-Aid for Scientific Research (B)

Allocation TypePartial Multi-year Fund
Section一般
Research Field Neurophysiology and muscle physiology
Research InstitutionKyorin University

Principal Investigator

AKAGAWA kimio  杏林大学, 医学部, 教授 (80129303)

Co-Investigator(Renkei-kenkyūsha) FUJIWARA Tomonori  杏林大学, 医学部, 准教授 (90255399)
SUGA Kei  杏林大学, 医学部, 講師 (30306675)
MISHIMA Tatsuya  杏林大学, 医学部, 助教 (40317095)
KOFUJI Takefumi  杏林大学, 医学部, 助教 (40365200)
NAKAYAMA Takahiro  杏林大学, 医学部, 助教 (90342823)
SAITO Ayako  杏林大学, 医学部, 実験助手 (80424109)
SANADA Masumi  杏林大学, 医学部, 実験助手 (70424108)
Project Period (FY) 2012-04-01 – 2015-03-31
Keywords神経伝達 / syntaxin1A / syntaxin1B / 機能分化 / 遺伝子ノックアウトマウス / グリア細胞 / BDNF
Outline of Final Research Achievements

With gene-knockout mice, functional difference between syntaxin1A(sy1A) and syntaxin1B(sy1B)in synaptic transmmission was investigted. We found that in sy1AKO glutamatergic and GABAergc transmission was normal but in sy1BKO frequency of mPSP was decreased, and reduction of ready releasable pool and increase of vesicle recycling were observed. In case of sy1A/1B double KO, synaptic transmission occurred following evoked stimulation but release of each synaptic vesicle was asynchronous. These results indicated that syntaxin1 was not essentially necessary for exocytotic process in synaptic transmission but regulated synchronous relaese of synaptic veiscles. Furthermopre, it was shown that sy1B regulated release of BDNF from glia cells, supporting neuronal development and survival.

Free Research Field

分子神経生物学

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Published: 2016-06-03  

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