拉莫三嗪对电刺激大鼠运动皮层惊厥模型干预的病理生理学研究

目的探讨拉莫三嗪对电刺激大鼠运动皮层惊厥模型干预的脑保护作用。方法建立电刺激大鼠运动皮层惊厥模型,将25只模型动物随机分为5组,拉莫三嗪高剂量组(37.5mg·kg-1·d-1)、拉莫三嗪中剂量组(25mg·kg-1·d-1)、拉莫三嗪低剂量组(12.5mg·kg-1·d-1)、阳性对照组(生理盐水5mg·kg-1·d-1)和阴性对照组(不给刺激仅给生理盐水5mg·kg-1·d-1)。除阴性对照组外,其他各组大鼠每天刺激2次并纪录惊厥阈值;实验各组每周记录一次大鼠在刺激前和刺激后的脑电图;6周末(42~43d)处死大鼠取脑组织行组织形态学检查。结果给电刺激后的各个实验组其惊厥阈值都呈现下降趋势,但拉莫三嗪药物组的惊厥阈值下降延迟,并且在实验末期相对稳定在一个较高水平,其脑电图的棘(尖)波指数也明显减少,组织学检查可见大鼠海马CA3区的神经元细胞损伤较轻。结论在持续6周的实验中,拉莫三嗪对电刺激大鼠运动皮层惊厥模型有脑保护作用,并呈剂量依赖。

Protection with Lamotrigine against electro-stimulated convulsion with collagen-induced arthriti

Objective To investigate whether Lamotrigine may provide protection against electro-stimulated convulsion of motor cortex in rat models. Methods The model of the convulsive threshold was prepared by direct cortex electric stimulation. Twenty-five model rats were randomized into 5 groups to receive Lamotrigine 37.5mg·kg^-1·d^-1, Lamotrigine 25mg·kg^-1·d^-1, Lamotrigine 12.5 mg·kg^-1·d^-1 or normal saline （stimulated and non-stimulated controls） by garvage, respectively. Except for the non-stimulated controls, all rats were stimulated twice daily and recorded for con- vulsion threshold. EEGs were recorded weekly before and after stimulation. After 6 weeks,brain tissues of the rats were removed for pathological study. Results While lowered convulsive threshold was found in all rats subjected to electro-stimulation, Lamotrigine intervention resulted in slower descending of the threshold which remained significantly higher than that in the normal saline group （electric stimulation） （P〈0.05）. Sharp and spike waves of EEG were obviously decreased in Lamotrigine groups. Compared with normal saline group （electric stimulation）, significantly milder pathological changes of hippocampus CA3 was noted in Lamotrigine groups. Conclusion Over six weeks, Lamotrigine showed obvious cerebro-protection against convulsion of motor cortex in a dose-dependent manner.