点燃癫痫模型中颞区脑组织GAD基因表达的研究  

Relationship between kindling model and the expression of GAD gene in temporal tissue

作　　者：田发发[1] 谢光洁[1] 杨期东[1] 陈主初[2] 吕冰清[1] 

机构地区：[1]中南大学湘雅医院神经内科,湖南长沙410008 [2]中南大学湘雅医院肿瘤研究所,湖南长沙410008

出　　处：《中风与神经疾病杂志》2002年第3期145-147,共3页Journal of Apoplexy and Nervous Diseases

摘　　要：目的　探索癫痫发生与谷氨酸脱羧酶 (GAD)基因表达的关系。方法　采用印防己毒 (PTX)腹腔注射致 SD鼠慢性点燃模型 ,将 SD鼠分为对照组、癫痫发作组、发作间期组和苯巴比妥钠干预组。 RT- PCR半定量方法检测颞区脑组织 GAD6 7和 GAD6 5m RNAs表达水平。结果　癫痫发作期和发作间期颞区脑组织 GAD6 7和 GAD6 5m RNAs表达水平较对照组均明显升高 (P<0 .0 5 ) ,以 GAD6 5m RNAs表达水平在发作期升高最明显 (P<0 .0 1) ,而药物干预组颞区脑组织 GAD m RNA表达水平无明显变化。结论　在该模型中 ,GAD基因表达水平改变与癫痫发作密切相关 ,提示 GABA能神经元的抑制功能增强是机体重要的内源性抗癫痫机制。苯巴比妥钠可以预防癫痫的发生 ,从而阻止脑组织 GAD基因表达代偿性增强。Objective To study the relationship between epileptic seizure and the expression of glutamate decarboxylase(GAD) gene. Methods RT PCR was used to determine the expression of GAD mRNAs in the temporal tissue of Sprague Dawley(SD) rats' kindled model. SD rats were devided randomly into four groups:Control group (Group A),Epilepsy group in ictal period (Group B),Epilepsy group in interictal period (Group C) and phenobarbital group (Group D). The kindling models of rats were induced by daily injection of picrotoxin (PTX) intraperitoneally. Results The levels of GAD 67 and GAD 65 mRNAs in Group B and Group C were significantly increased than those in Group A (P<0.05),especially the GAD 65 mRNA expression in Group B(P<0.01). There was no changes in GAD 67 or GAD 65 mRNAs between Group A and Group D. Conclusion The changes of GAD mRNAs are closely related to epileptic seizure. The results suggest the augmented GABA ergic neurotransmission is the selfprotective and anticonvulsive mechanism in this model. Phenobarbital sodium can protect SD rats daily injected PTX intraperitoneally from seizure.

关 键 词：癫痫 谷氨酸脱羧酶 基因表达 RT-PCR SD鼠 慢性点燃模型 颞区脑组织 

分 类 号：R742.1[医药卫生—神经病学与精神病学]