| Project/Area Number |
23650170
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Neuroscience in general
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| Research Institution | Kyoto Sangyo University |
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Principal Investigator |
HAMA Chihiro 京都産業大学, 総合生命科学部, 教授 (50238052)
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| Co-Investigator(Kenkyū-buntansha) |
NAKAYAMA Minoru 京都産業大学, 総合生命科学部, 助教 (40449236)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
Fiscal Year 2013: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2012: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2011: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Keywords | てんかん / SRPX2 / Hig / ショウジョウバエ / シナプス / アセチルコリン受容体 / シナプス間隙 / マトリックス / 言語失調 / 細胞骨格タンパク質 / 神経発生 / コリン作動性 / hikaru genki / srpx2 / 行動 / 神経 / 病気 |
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| Research Abstract |
Human SRPX2 gene is responsible for the congenic Rolandic epilepsy and oral dyspraxia. To understand the molecular mechanism underlying these genetic defects, we study Drosophila as a model system, because a variety of genetic tool is available.
As the Drosophila hig gene is similar to SRPX2 in domain organization, hig is the target of our genetic analysis. The encoded protein Hig is extracellularly secreted and specifically localized to the synaptic cleft of cholinergic synapse in the brain. The absence of Hig results in reduced locomotion and longevity, and also causes a decrease in the amount of acetylcholine receptor subunits Da6 and Da7 in the synaptic regions. Thus, Hig regulates the organization of cholinergic synaptic structure. This finding indicates a possible avenue for understanding the mechanisms underlying Rolandic epilepsy in the human brain, and also for providing insights into how extracellular matrix proteins organize synaptic structures.
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