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2016 Fiscal Year Final Research Report

Analysis for mechanism of spontaneous seizures in a rat model of multiple prenatal freeze lesioning and development of novel treatment for epilepsy focusing on connexin

Research Project

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Project/Area Number 26461273
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Neurology
Research InstitutionKurume University (2016)
Kyushu University (2014-2015)

Principal Investigator

Kamada Takashi  久留米大学, 医学部, 助教 (70614460)

Project Period (FY) 2014-04-01 – 2017-03-31
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
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.

Free Research Field

神経内科学(てんかん)

URL: 

Published: 2018-03-22  

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