Functional difference between syntaxin1 isoforms in synaptic transmission
| Project/Area Number |
24300142
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Partial 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 | Kyorin University |
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Principal Investigator |
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| 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)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥18,850,000 (Direct Cost: ¥14,500,000、Indirect Cost: ¥4,350,000)
Fiscal Year 2014: ¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2013: ¥6,500,000 (Direct Cost: ¥5,000,000、Indirect Cost: ¥1,500,000)
Fiscal Year 2012: ¥7,670,000 (Direct Cost: ¥5,900,000、Indirect Cost: ¥1,770,000)
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| 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 / シンタキシン１A / シンタキシン１Ｂ / 速い神経伝達物質放出過程 / 遅い神経伝達物質放出過程 / 自閉性障害 / haploid / シンタキシン１B / シナプス伝達 / 開口放出 / 神経成長因子 / シンタキシン1A / シンタキシン1B / ノックアウトマウス |
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| 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.
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Report
(4 results)
Research Products
(17 results)
