中文摘要：

目的观察经皮三叉神经电刺激对匹罗卡品诱发癫痫持续状态（sE）大鼠海马神经元的保护作用及对大鼠谷氨酸脱羧酶（GAD65／67）表达的影响。方法通过匹罗卡品建立癫痫点燃模型（即慢性癫痫模型），采用随机数字表法将其分为治疗组及模型组，同时选取正常大鼠纳入空白对照组进行对照。治疗组及模型组大鼠于制模后分别给予三叉神经电刺激或假刺激持续1个月。于电刺激结束并再次诱发sE后6h、24h、48h及72h分别采用TUNNEL和Nissl染色观察各组大鼠SE后海马神经元原位凋亡及脱失情况；于电刺激结束后24h、72h、1周、2周及4周时分别采用免疫组化法检测各组大鼠GAD65／67表达情况。结果sE后24h、48h及72h治疗组海马区TUNNEL阳性细胞、Nissl受损细胞均较模型组显著减少（P〈0．05），并以SE后72h治疗组减少幅度尤为显著（P〈0．05）。电刺激结束后24h、72h、1周、2周及4周时治疗组GAD65／67表达均较模型组明显增强（P〈0．05），治疗组GAD65于电刺激结束72h～1周时达到峰值，随后缓慢下降，于电刺激结束4周时接近正常水平。治疗组及模型组大鼠GAD67表达均未见明显峰值，治疗组GAD67表达至电刺激结束4周时仍显著强于模型组水平（P〈0．05）。结论经皮三叉神经电刺激治疗对癫痫大鼠海马神经细胞具有保护作用，增强脑内抑制功能可能是其发挥脑保护及抗癫痫作用机制之一。

英文摘要：

Objective To study any protection against hippocampal neuron damage induced by epilepsy （SE） provided by transcutaneous stimulation （TNS） of the trigeminal nerve and to document any effect of such stimulation on the expression of glutamic acid decarboxylase （GAD） 65/67. Methods Pilocarpine injection was used to induce epilepsy in healthy male Sprague-Dawley rats which were then randomly divided into a treatment group and a model group. Rats which had not received the pilocarpine injection served as normal controls. In the treatment group the rats were given eleetrostimulation for one month after the first spontaneous seizure following the injection of pilocarpine. In the model group they were given sham TNS for one month. After the month of stimula- tion, immunohistochemistry was used to detect the expression of GAD65/67 in the hippoeampus. Terminal deoxy- nucleotidyl transferase-mediated dUTP nick end labeling （TUNEL） assays and Nissl staining were applied to deter- mine apoptosis and neuron loss in the hippocampus. Results Significantly less apoptosis was observed in the treatment group than in model group at 24 h, 48 h and 72 h post-injection. Compared to the model group, average GAD65/67 expression had increased significantly in the treatment group at 24 h, 72 h, 1 week, 2 weeks and 4 weeks post-stimulation. GAD65 expression reached its peak from 72 h to 1 week post-stimulation, then decreased to the level of the control group by 4 weeks post-stimulation. The expression of GAD67 remained elevated at all the time points employed. Conclusions TNS can significantly protect hippocampal neurons from damage in epilepsy, at least in rats. The underlying anti-epileptic and neuroprotective mechanisms may involve increased inhibitory transmission induced by the stimulation.