海人酸致痫大鼠海马CA_3区神经元线粒体损伤及妥泰的保护作用  

Mitochondrial damage and neuroprotective effect of topiramate in hippocampal CA_3 neurons during kainic acid induced status epilepticus in rats

作　　者：孙建英[1] 冯延秋[2] 迟兆富[1] 吴伟[1] 

机构地区：[1]山东大学齐鲁医院神经内科,山东济南250012 [2]滨州医学院附属医院,山东滨州256603

出　　处：《山东大学学报（医学版）》2006年第6期560-563,共4页Journal of Shandong University:Health Sciences

基　　金：山东省自然科学基金资助课题(Y2001C10)

摘　　要：目的:观察海人酸(KA)诱导的癫痫持续状态(SE)大鼠海马CA3区神经元线粒体超微结构的损伤及妥泰(TPM)的保护作用。方法:用TPM干预。用KA诱导大鼠SE 2 h,并评估大鼠的行为学表现。于SE终止后3 h制作脑切片,光镜观察神经元的大体损伤,电镜进一步观察线粒体的超微结构。结果:KA组出现痫性发作的时间为注入KA后(15.3±4.6)min,而TPM组为(26.1±5.3)min,两组差异有统计学意义(P<0.05)。KA组大鼠的线粒体损伤为(3.67±0.34)级,TPM组为(2.48±0.21)级,两组差异有统计学意义(P<0.05)。结论:KA诱导的SE可导致海马神经元线粒体损伤,妥泰对此具有抑制作用。Objective： To observe the mitochondrial damage in the hippocampal CA3 neurons during kainie acid （KA） induced status epileptieus（SE） and the neuroprotective effect of topiramate （TPM） in rats. Methotis： Thirty male Wistar rats were randomly divided into TPM, KA, and NS （normal saline） groups. TPM group was pretreated with TPM for 15days. SE was induced by KA in the first two groups for 2 hours and the third group was given the same volume of NS. The seizure behaviors of rats were evaluated. Three hours later the rats were killed and the brain sections were made. We observed the neuronal damage with light microscope and the mitochondrial ultrastructure with electron microscope. Results： In KA group, SE was induced（ 15.3 ±4.6） minutes after the injection of KA, while in TPM group, （26.1 ± 5.3） minutes, and the difference was significant （ P 〈 0.05）. The damage degree of mitochondrial ultrastructure was 3.67 ±0.34 and 2.48 ± 0.21 in KA and TPM groups respectively （P 〈 0.05）. Conclusion： Our results suggested that KA-induced SE can cause mitochondrial ultrastructure damage in the hippocampal neurons, and TPM has neuroprotective effect against this damage.

关 键 词：癫痫持续状态 线粒体 超微结构 妥泰 

分 类 号：R742.1[医药卫生—神经病学与精神病学]