| Project/Area Number |
26461273
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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 |
Neurology
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| Research Institution | Kurume University (2016)
Kyushu University (2014-2015) |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
高瀬 敬一郎 九州大学, 医学研究院, 共同研究員 (00467903)
山口 浩雄 九州大学, 大学病院, 講師 (00701830)
重藤 寛史 九州大学, 医学研究院, 共同研究員 (50335965)
真崎 勝久 九州大学, 医学研究院, 助教 (90612903)
|
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | てんかん / 皮質異形成 / コネキシン蛋白群 / てんかん動物モデル / 動物モデル / 海馬 |
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| Outline of Final Research Achievements |
In a previous study we created an animal model with multiple FCD, produced by freeze lesioning during embryonic development, showing hippocampal spontaneous seizures. Recently, involvement of chronic inflammation and excessive intercellular network with connexin has been pointed out as a mechanism for development of epilepsy. In this study, we analyzed the expression of receptors and inflammatory cytokines related to chronic inflammation and connexin in the hippocampus and cortex after the onset of epilepsy in this animal model. Semiquantitative densitometry of immunoreactivity revealed increased IL-1β, Cx32, Cx43 expression in hippocampus and GFAP, TLR4, IL-1β, Cx32, Cx36, Cx43 expression in lesioned cortices. The mechanism for development of hippocampal epileptogenesis with cortical dysplasia was suggested to be an abnormal excitatory network circuit involving chronic inflammation and connexin.
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