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作 者:孙建英[1] 迟兆富[1] 吴伟[1] 刘学伍[1] 赵秀鹤[1]
出 处:《神经解剖学杂志》2006年第2期219-223,共5页Chinese Journal of Neuroanatomy
基 金:山东省自然科学基金(Y2001C10)资助项目
摘 要:为了观察海人酸诱导的癫痫持续状态(SE)大鼠海马CA3区神经元线粒体与细胞核超微结构的损伤及caspase3的表达变化,本研究采用海人酸诱导2h,导致大鼠出现SE,然后分别于SE终止后第3、12、24h制作脑切片,用电镜观察线粒体和细胞核的超微结构,并用免疫组化方法检测caspase3的表达。SE终止后3h,电镜下可见线粒体的嵴肿胀和膜崩解。细胞核于SE后24h出现染色质显著边集的改变。caspase3的表达在SE后12h开始增加(与对照组相比,P<0.05),于第24h明显增高(P<0.01)。上述结果提示,在实验性SE模型中,线粒体超微结构的损伤早于caspase3的表达增高及细胞核的改变,线粒体的损伤可能是SE后神经元损伤的关键环节。In order to observe the mitochondrion and nucleus ultrastructural damage and the change of caspase-3 expression in the neuron of hippoeampal CA3 region during kainic acid (KA) induced status epilepticus (SE) in the rat, SE model rats were made by administrating KA for 2 h and terminated with diazepam. 3, 12 and 24 h later, the rats were killed and the brain sections were made. The uhrastructure of the mitochondrion and nucleus was observed with electron microscope, and caspase-3 expression was examined with immunohistochemical staining. Three hours after SE, mitochondrion showed swelling cristae and ruptured membrane, and the nucleus showed significant margination of the chromatin at 24 h. Caspase-3 expression began to increase at 12 h after SE (compared with the control group, P 〈 0.05 ) , and increased markedly at 24 h ( P 〈 0.01 ). The present results suggest that the ultrastructural damage of mitochondrion occurred in the early period after experimental SE, followed by nucleus change and the increment of caspase-3 over expression, which could be critical in neuronal damage after SE.
关 键 词:癫痫持续状态 线粒体 细胞核 超微结构 caspase-3
分 类 号:R742.1[医药卫生—神经病学与精神病学]
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