Effects of antisense glutamic aciddecarb0xylase oligodeoxynucleotide on epileptic rats induced by pentylenetetrazol

作     者：何小华 李文鑫 王伟 阮旭中 张梁 He Xiaohua;WANG Wei;Ruan Xuzhong;LI Wenxin;ZHANG Liang

作者机构：武汉大学生命科学院生物技术系武汉430070 同济医科大学附属同济医院神经内科武汉430030 

出 版 物：《Chinese Medical Journal》 (中华医学杂志（英文版）)

年 卷 期：2002年第115卷第3期

页      面：425-429页

核心收录：

学科分类：1007[医学-药学(可授医学、理学学位)] 1006[医学-中西医结合] 100706[医学-药理学] 1002[医学-临床医学] 100204[医学-神经病学] 10[医学] 100602[医学-中西医结合临床] 

基　　金：supported by the National Nature Science Foundation of China(No.39700047) 

主　　题：Animals Electroencephalography Epilepsy Glutamate Decarboxylase Hippocampus Isoenzymes Kindling (Neurology) Male Oligonucleotides, Antisense Pentylenetetrazole Rats Research Support, Non-U.S. Gov't gamma-Aminobutyric Acid 

摘      要：OBJECTIVE: To investigate the effects of antisense glutamic acid decarboxylase (GAD(67)) oligodeoxynucleo-tide (ODN) on behavior, seizure threshold and EEG of hippocampus in the epileptic rats induced by pentylenetetrazol (PTZ). METHODS: A model of chronic epilepsy in rats was established by PTZ. The inhibition of GAD(67) mRNA expression in hippocampus was selectively induced by antisense oligodeoxynucleotide of GAD(67). The effect of antisense GAD(67) ODN on behavior, seizure threshold and EEG recording of kindled rats was examined. RESULTS: Antisense GAD(67) ODN could inhibit the expression of GAD(67) mRNA and the concentration of GABA. It also could significantly shorten the latencies of seizure and increase the level of seizure and the frequency of epileptiform discharges. CONCLUSION: The gene of GAD(67) may be an anti-seizure gene, which might inhibit epileptiform discharge. The treatment of epilepsy by GAD(67) gene will have a bright future.