摘要
目的 探讨大鼠杏仁核点燃癫痫后脑组织谷氨酸脱羧酶（ＧＡＤ）ｍＲＮＡ的表达及其在癫痫发作后表达变化的意义。方法 通过建立与人类癫痫发生、形成具有高度相似性的杏仁核点燃大鼠癫痫模型，采用原位杂交技术检测癫痫鼠颞叶及海马组织不同点燃时程ＧＡＤ６７ ｍＲＮＡ表达。结果 点燃后１ｄ，ＧＡＤ６７ｍＲＮＡ表达增多并且表达信号增强，至７ｄ时达高峰，以后表达逐渐下降，但在点燃后４９ｄ，表达仍高于正常，与对照组及手术对照组相比有统计学差异。结论 在慢性癫痫发作中，ＧＡＢＡ能神经元的活性增强，考虑是由于癫痫过程中兴奋性增强，引起ＧＡＢＡ能神经元抑制功能代偿性增加的结果。即癫痫发作后ＧＡＢＡ能神经元介入的抑制功能代偿性增加的，这可能是机体内源性抗癫痫机制增强的一种反应。
Objective To explore expression of GAD67 mRNA in the brain cells of the rats after epilesy kin- dled by electrical amygdala. Methods The model of rat epitepsy was made by electrifing amygdala, expression of GAD67 mRNA in hippocampus and temporal lobe tested by situ hybridization during different times. Results Ex- pression of GAD mRNA began to up-regulate at 1d following kindling. With the development of seizure, the ex- pression of GAD mRNA up-regulated gradually and reached its peak at 7d following kindling, then attenuated, but still above the normal level. There was significant difference between control and epileptic group. Conclusion The results suggest that the activity of GABA ergic neurons enhanced in chronic seizures. Hence, the enhance of GABA ergic neurons may be die to the compensative enhance excitability during seizure, which may he a kind of introgenetic antiepileptic reaction.
出处
《中风与神经疾病杂志》
CAS
CSCD
北大核心
2001年第6期344-346,共3页
Journal of Apoplexy and Nervous Diseases
