| Project/Area Number |
24592169
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Cerebral neurosurgery
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| Research Institution | Kagoshima University |
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Principal Investigator |
HANAYA Ryosuke 鹿児島大学, 医学部・歯学部附属病院, 講師 (60304424)
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| Co-Investigator(Kenkyū-buntansha) |
YUNOUE Syunji 鹿児島大学, 医歯(薬)学総合研究科, 研究員 (20404478)
SUGATA Sei 鹿児島大学, 医歯(薬)学総合研究科, 研究員 (70437961)
ARITA Kazunori 鹿児島大学, 医歯(薬)学総合研究科, 教授 (90212646)
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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 |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | てんかん原性 / シナプス小胞蛋白 / SVA2 / Synaptotagmin-1 / FDG-PET / てんかん / SV2A / SNARE関連蛋白 / sinaptotagmin-1 / SNARE蛋白 |
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| Outline of Final Research Achievements |
We immunohistochemically evaluated the role of synaptic vesicle protein, SV2A about the expression of epilepsy using specimens of surgically treated-patients. SV2A decreased in the wide area of the brain, and the decrease of synaptotagmin-1 localized around epilepsy focus, whereas SNARE-related protein disorder would participate in the formation of epileptogenicity. Hypometabolism of FDG-PET, which indicated brain dysfunction overlapped in the decease of SV2A. SV2A mediated synaptic vesicle-releasing mechanism would be disturbed in dysfunctional brain around epileptogenic area, it was suggested that.
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