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J Korean Epilepsy Soc. 2007 Jun;11(1):15-24. Korean. Original Article.
Yi SW , Kim KS , Kim MJ , Kim JK , Yoo BG , Ahn JH , Chang HK .
Department of Neurology, Kosin University College of Medicine, Busan, Korea. nekim@ns.kosinmed.or.kr
Department of Pathology, Kosin University College of Medicine, Busan, Korea.
Abstract

PURPOSE: To investigate whether c-Jun, Bcl-2 and Bax expressions are altered in rat hippocampus after kainic acid (KA)-induced seizures, and to determine whether such changes correlate with apoptotic cell death. METHODS: Forty male Sprague-Dawley rats were used. Thirty rats were assigned to the experiment group, and 10 rats the control. KA (20 mg/kg) was injected once intraabdominally. The behavioral patterns were observed after the injection. The rats' brain was extracted 4, 24, and 72 hours after KA injection. c-Jun, Bcl-2 and Bax expression were evaluated by immunohistochemistry, and apoptosis by TUNEL staining. The expression of c-Jun, Bcl-2 and Bax at each hippocampal region were compared, and the relationship between c-Jun, Bcl-2 and Bax expression, and apoptosis was investigated. RESULTS: c-Jun expression was increased at CA1, CA3 and CA4 regions 4 hours after the injection, and the increased expression was continued to 72 hours at CA3 region. Bcl-2 expression was increased at CA1, CA3 and CA4 regions 4 and 24 hours after the injection, and the increased expression was continued to 72 hours at CA3 region. Bax expression was increased at CA3 and CA4 regions 4 hours after KA injection, and the increased expression was continued to 72 hours at CA3 region. Apoptosis was significantly increased at CA3 region 4 hours after KA injection. CONCLUSION: c-Jun expression was increased in hippocampus after KA-induced seizures, and cell death-regulating proteins Bcl-2 and Bax expression, and apoptosis were increased at similar regions. These results suggest that c-Jun might be activated in KA-induced apoptotic cell death mechanism.

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