| Project/Area Number |
23592106
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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 | Juntendo University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
SUGANO Hidenori 順天堂大学, 医学部, 准教授 (90265992)
NISHIMURA Kinya 順天堂大学, 医学部, 教授 (80164581)
ARAI Hajime 順天堂大学, 医学部, 教授 (70167229)
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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 |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2013: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2012: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2011: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 側頭葉てんかん / てんかん原性 / 神経細胞新生 / 炎症メディエーター / 海馬硬化症 / パッチクランプ / トル様受容体 / 新生神経細胞 / 慢性炎症 / Patch-clamp / てんかん原生 / 海馬 / 神経新生 / てんかんモデルマウス / ピロカルピン / GFP / レベチラセタム |
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| Research Abstract |
Epileptic seizures cause continuous pathological and electrophysiological hippocampul (HIPP) changes, inducing epileptogenesis (EG). Control of this process has not been found until now. Aiming pharmacological control on induced EG, we evaluated treatment effect of levetiracetam (LEV) on pathological changes in epileptic mice HIPPi where continuous LEV treatment suppressed epilepsy-induced neurogenesis. Preventive LEV treatment potentially inhibits such pathological changes. Cellular and molecular mechanisms of EG induction, however, remain unclear. Brain inflammatory mechanisms activation received recently broad attention as a factor in acquired EG. Our preliminary clinical study suggested elevated expression of HMGB1 and TLR4 in sclerotic HIPPi, indicating HMGB1-TLR4 pathway involvement in human EG. More, in human EG HIPP, HMGB1 involved consequently TLR4, probably in relation to HIPP sclerosis induction (CA1> DG> CA2) and atrophy,
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