Objective To approach the effectiveness of DBS on the expression of the delta subunit of the extrasynaptic GABAA receptor in the kainic acid induced rat model, and to provide reference for the pathogenesis of epilepsy and the therapeutic mechanism of DBS. Methods SD rats ( n = 24, male) were randomized into the control group, epilepsy group and DBS treatment group. Cohering the EEG and pathology, the effectiveness of DBS on the epilepsy and the distribution and expression of the delta subunit of the extrasynaptic GABAA receptor in a kainic acid induced rat model were analyzed. Results The seizure frequency in the DBS treatment group (6.01 ± 4.87, n = 8) was significantly lower than that in the epilepsy control group (17.31 ±4.59, n = 8) (P ＜0.05). DBS inhibited the abnormal discharges in the hippocampus of epileptic rats. Hippocampal neurons loss and glial cells hyperplasia in the DBS treatment group (463.62 ± 38.41,n = 8 ) were significantly lighter than those in the epilepsy group (357.12 ± 20.50, n = 8) (P ＜ 0.05 ). The δ subunit of extrasynaptic GABA receptor in the brain of normal control group mainly expressed in the hippocampus ( IOD = 30.96 ± 2.73, n = 8) and ventral lateral thalamic nucleus ( IOD = 32.85 ± 2.35, n = 8 ).The expression of δ subunit of extrasynaptic GABA receptor in hippocampal epileptic rats (IOD = 12.31 ± 1.72, n = 8 ) and ventral lateral thalamic nucleus ( IOD = 22.39 ± 1.94, n = 8) significantly decreased. In the DBS treatment group, the expression of the δ subunit of extrasynaptic GABA receptor in ventrolateral thalamic nucleus ( IOD = 35.91 ± 3.97, n = 8 ) and hippocampus ( IOD = 22.74 ± 2.08, n = 8 ) were significantly increased compared with the the epilepsy group ( P ＜ O. 05). Conclusion STN DBS treatment can inhibit the epilepsy and alter the abnomal discharge in hippocampus by increasing the expression of the delta subunit of the GABA receptor in the thalamencephal and hippocampus.%目的 研究DBS治疗对海人酸癫痫大鼠大脑中突触外GABAA受体δ亚基分布与表达的影响,为癫痫的发病机制与DBS的治疗机制的研究提供参考.方法 雄性SD大鼠24只,随机分为正常对照组、癫痫组、DBS治疗组.通过免疫组织化学方法检测突触外GABAA受体δ亚基在大鼠大脑中的分布与表达量的变化.结合大鼠脑电信号的采集分析以及病理形态学观察,分析DBS在癫痫治疗中的作用以及对突触外GABAA受体δ亚基的影响.结果 DBS治疗组大鼠癫痫发作次数(6.01±4.87,n=8)明显低于癫痫对照(17.31±4.59,n=8),P＜0.05;DBS治疗可有效抑制癫痫大鼠海马异常放电;DBS治疗组(463.62±38.41,n=8)大鼠海马神经元坏死及胶质细胞增生程度较癫痫组轻(357.12±20.50,n=8)(P＜0.05);正常对照组大鼠脑组织突触外GABA受体δ亚基主要分布在海马(IOD=30.96±2.73,n=8)与丘脑腹外侧核(IOD=32.85±2.35,n=8).癫痫组大鼠脑组织海马(IOD=12.31±1.72,n=8)及丘脑腹外侧核(IOD=22.39±1.94,n=8)突触外GABA受体δ亚基表达下降.DBS治疗组的丘脑腹外侧核(IOD=35.91±3.97,n=8),海马区(IOD=22.74±2.08,n=8)突触外GABA受体δ亚基表达比癫痫组表达增高(P＜0.05).结论 丘脑底核DBS治疗可以通过改变大脑突触外GABA受体δ亚基的表达,抑制癫痫大鼠海马的异常放电,减轻癫痫大鼠海马神经元病理变化,起到对癫痫的治疗作用.
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