海人酸颞叶癫痫模型及丙戊酸钠治疗作用的观察  

Therapeutic effect of sodium valproate on kainic acid induced temporal lobe epilepsy model

作　　者：张川[1] 申长虹[1] 

机构地区：[1]天津医科大学总医院神经外科,300052

出　　处：《中国现代神经疾病杂志》2004年第5期309-312,共4页Chinese Journal of Contemporary Neurology and Neurosurgery

基　　金：天津市高等学校科技发展基金资助项目(01-20806)

摘　　要：目的建立海人酸癫痫动物模型并给予丙戊酸钠治疗,探讨其治疗作用。方法42只Wistar大鼠置于立体定向仪上,于右侧海马注射海人酸制备大鼠癫痫模型。根据癫痫发作病程,随机分为急性期、静止期、慢性期等实验组;另设丙戊酸钠治疗组,分别于海人酸注射后24h和自发性癫痫出现后给予丙戊酸钠治疗。在实验过程中以视频录像监测大鼠症状的改变,深部脑电图观察癫痫的病理过程及丙戊酸钠治疗前后脑电活动的改变。组织切片经Nissl和Timm染色观察海马神经元数目、苔藓状纤维发芽。结果(1)电生理学改变:海人酸注射后数分钟大鼠即出现癫痫发作并呈现急性期、静止期和慢性期等病变过程。脑电图于急性期和慢性期均表现为典型的癫痫发作电活动及发作间期表现。(2)病理学改变:海马神经元死亡主要出现在急性期,以实验侧CA3、CA4区最为明显,齿状回无明显神经元缺失。Timm染色显示从静止期开始出现苔藓状纤维发芽并进行性增加。(3)丙戊酸钠治疗前后症状的改变:早期应用丙戊酸钠治疗可抑制癫痫发作及其症状的发展;出现自发性癫痫后丙戊酸钠的治疗效果欠佳,停药后症状再次出现。结论海人酸模型是模拟人类颞叶癫痫较为理想的动物模型。早期丙戊酸钠治疗效果较好,否则不能有效控制癫痫。Objective To establish the kainic acid induced model of temporal epilepsy in rat and treat with sodium valproate, and study on its therapeutic effects. Methods The epilepsy model was established in 42 Wistar rats by injection of kainic acid into right hippocampus by means of stereotaxic instrument.The rats were randomly divided into experimental groups eg acute phase, resting phase and chronic phase group according to the epilepsy course, and sodium valproate treatment group. Sodium valproate was administrated in 24 hours after injection of kainic acid or attack of spontaneous epilepsy in different groups respectively. The symptoms of rats were monitored by video recording. The electrical activity changes of brain were observed by EEG during epileptic course and before or after treatment with sodium valproate. The histological slides were stained by Nissl's and Timm's staining for study the hippocampus neurons amount and budding of lichenoid fibers. Results 1) Electrophysiological changes: In a few minutes after injection of sodium valproate, the epileptic attack occurred and presented the course of acute, resting and chronic phases. The typical electrical activity of epileptic attack and manifestations of inter attack phase were found in EEG during acute and chronic phases. 2) Pathological changes: Death of hippocampus neurons was mainly found in acute phase and obviouly found in CA3, CA4 area on experimental side, but significant neuron defect was not found in dentate gyrus. The budding of lichenoid fibers were found at the begining of resting phase and increasing progressively by Timm's staining. 3) Symptom changes before and after sodium valproate treatment: Epileptic attack and its symptom development could be inhibited by early sodium valproate treatment. But the therapeutic effect was poor when sodium valproate treatment was administrated after the occurrence of spontaneous epilepsy and recurrence of symptoms would appear after withdrawal. Conclusion The kainic acid induced epilepsy model is an

关 键 词：颞叶癫痫 丙戊酸钠 药物治疗 动物模型 海人酸模型 

分 类 号：R742.1[医药卫生—神经病学与精神病学] R971[医药卫生—临床医学]