2014 Fiscal Year Final Research Report
Functional difference between syntaxin1 isoforms in synaptic transmission
Project/Area Number |
24300142
|
Research Category |
Grant-in-Aid for Scientific Research (B)
|
Allocation Type | Partial Multi-year Fund |
Section | 一般 |
Research Field |
Neurophysiology and muscle physiology
|
Research Institution | Kyorin University |
Principal Investigator |
|
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
|