摘要
目的:探讨大鼠癫痫发作时海马神经元凋亡变化。方法:采用红藻酸氨(KA)诱导大鼠癫痫发作模型,观察行为学及脑电图变化;用神经元尼氏体亚甲蓝特殊染色法观察大鼠癫痫发作时海马CA1区神经元损害情况;用原位细胞凋亡检测法观察癫痫发作时海马CA1区神经元凋亡情况及苯巴比妥干预后神经元凋亡的变化。结果:KA注射后大鼠出现严重边缘性惊厥,脑电图表现为持续性癫痫样放电。海马细胞在KA注射后8h开始出现凋亡阳性细胞,48h达高峰,主要表现在CA1区锥体细胞,经苯巴比妥干预后凋亡细胞明显减少。结论:癫痫发作后的迟发性神经元死亡很可能经由凋亡途径,早期终止癫痫发作可抑制海马神经元凋亡。
Objective:To investigate changes of Hippocampus neurons apoptosis cell upon Kainic acid(KA)-induced seizure in rats.Method:We set up an experiment in KA model of limbic seizure in rats,the electroencephalogram(EEG)and behaviour changes of rat were simultaneously observed.The neuronal damage in the CA1section of the hippocampus after seizure was observed by Nissel body stain mothed;Apoptosis was detected by in situ end-labeling of fragmented DNA using the terminal deoxynucleotidyltransferase reaction(TUNEL);and to explore the changing of numbers of apoptosis cells in rat hippocampus with phenobarbital injection i.c.v.before KA.Result:All rats of KA-induced group exhibited limbic convulsions.The EEG recordings also showed electrical seizure activities.The numbers of apoptosis cell of CA1section significantly increased in rat hippocampus at8h,24h,48h and72h post-KA treatment(P<0.01).With phenobarbital injection i.c.v.,the numbers of apoptosis cell of CA1section significantly decreased in rat hippocampus at48h(P<0.01).Conclusion:The delayed neuronal deaths after KA-induced seizure were possibly in part caused by apoptosis.The inhibition of neuronal apoptosis was assumed to be a neuroprotective mechanism of stoping seizure as early as possible.
出处
《中国康复医学杂志》
CAS
CSCD
2003年第11期670-672,共3页
Chinese Journal of Rehabilitation Medicine