期刊文献+

锂-匹罗卡品致大鼠癫癎持续状态后脑内神经元的凋亡 被引量:1

Neuron apoptosis in rats after Lithium-Pilocapine-induced status epilepticus
下载PDF
导出
摘要 探讨癫持续状态 (StatusEpilepticus,SE)时细胞凋亡的发生及其与海马硬化的关系。采用锂 匹罗卡品诱发大鼠SE模型 ,在SE的不同时点采大鼠脑标本 ,利用TUNEL染色方法检测大鼠海马皮质神经元的凋亡出现情况。结果发现 ,正常对照组大鼠大脑皮质可见散在的TUNEL阳性细胞 ,海马区未见TUNEL阳性细胞。SE1h ,皮质TUNEL阳性细胞数即开始增加 ,SE后 8h ,海马区开始出现TUNEL阳性细胞 ,SE后 1d ,大脑皮质TUNEL阳性细胞数开始明显增加 ,海马区也可见到较多TUNEL阳性细胞。SE后 5d ,皮质及海马的TUNEL阳性细胞数达到高峰。 7d时皮质及海马TUNEL阳性数均明显下降。结果提示 ,SE可引起神经元凋亡 ,5d时达到高峰 ,7d时已明显下降。神经元凋亡与SE引起的迟发性神经元死亡有关 ,并参与了海马硬化的形成。 This study aimed to investigate the occurrence of neuronal apoptosis in rats with status epilepticus (SE).The SE models induced by lithium and pilocapine were established with Wistar male rats. The occurrence of neuronal apoptosis was observed by terminal deoxynucleotidal transfers mediated dUTP biotin nick end labeling(TUNEL)staining .The results indicated that in the normal control rats, TUNEL positive neurons can be found sporadically in the brain cortex and can not be found in hippocampus .The number of apoptotic neurons in the cortex increased significantly 1 day after SE, a lot of apoptotic neurons were also seen in the hippocampus .The number of apoptotic neuron peaked at 5 day,significantly decreased at 7 day.In conclusion:1.SE can cause neuronal apoptosis.2.Neuronal apoptosisis correlated to delayed neuronal death and participates in hippocampal sclerosis. \[
作者 魏昕 高旭光
出处 《中国神经科学杂志》 CSCD 2002年第4期715-718,共4页
关键词 锂-匹罗卡品 神经元 细胞凋亡 癫痫持续状态 海马硬化 动物模型 TUNEL染色方法 apoptosis status epilepticus(SE) hippocampal sclerosis
  • 相关文献

参考文献2

共引文献21

同被引文献8

引证文献1

二级引证文献7

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部