颞叶癫痫大鼠模型的建立及长期癫痫敏感性的研究

目的 探讨立体定向手术建立大鼠颞叶癫痫模型的方法及模型永久癫痫敏感性的病理学基础。方法 按公斤体重计算的海人酸通过立体定向手术一次性注入大鼠的海马组织,于手术后摄像观察大鼠的癫痫发作情况8周,同时,于发作后6h、1d、3d、5d、7d及2周、3周、4周、5周、6周、7周和8周检查海马组织的形态学变化。结果 手术后的大鼠在经历“湿狗样抖动”、口唇和头的自运动症、前肢抽搐、后肢抽搐后,进入强直一阵挛性全身发作,之后,每周均有自行发作。海马的病理改变为神经元缺失、胶质细胞增生。结论 立体定向手术建立的大鼠颞叶癫痫模型发作形式及病理学基础与人类的颞叶癫痫基本一致,同时,耗资较系统给药大大降低。海马神经元的缺失、胶质细胞增生是模型长期癫痫敏感性的基础。

Establishment of temporal epilepsy models and its permanent epilepsy sensitivity

OBJECTIVE: To explore a better method to establish an animal model of temporal epilepsy in rat and study the pathological basis of permanent epilepsy sensitivity. METHODS: Kainic acid (KA) with the dosage calculated according to the body weight was injected into 30 Wistar rats' hippocampuses by stereotactic operation. Videotape recording was used to record the seizures for 8 weeks. Two rats were randomly selected to undergo craniotomy and electroencephalography and then were killed to have their brains to be taken out to undergo slicing, staining, and histological examination 6 hours, 1 days, 3 days, 5 days, 7 days, 2 weeks, 3 weeks, 4 weeks, 5 weeks, 6 weeks, 7 weeks, and 8 weeks respectively after operation. RESULTS: Thirty minutes after the rats awoke from anesthesia, wet-dog shakes, lips and head self-movements, convulsion of forelimbs and hind limbs occurred successively. The seizures were paroxysmal with increased intervals during which, however, the rats still showed sluggish. Twenty-four hours after the rats' behavior recovered to normal. Then the seizure occurred 1 approximately 3 times every week. Epileptic waves were recorded in the hippocampus, striate body, cerebral cortex, and olfactory bulb from 5 hours to 2 months after the establishment of model. CONCLUSION: The seizure pattern and pathological basis of temporal epilepsy in the rat model established by stereotactic management were almost the same as those in human beings. Stereotactic method significantly decreased the needed dosage of KA and the cost in comparison with systematic injection. Loss of hippocampus neurons and hyperplasia of gliocytes are the basis of the permanent epilepsy sensitivity in the animal model.