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目的探讨缝隙连接抑制剂对海人藻酸(KA)致动物模型脑电活动的抑制作用。方法用电生理学的方法对比观察缝隙连接抑制剂连接蛋白拟似肽(CMP)及甘珀酸(CAR)对KA致后不同时间段大鼠皮层脑电活动的抑制作用。结果与生理盐水组比较,CMP及CAR均可使潜伏期明显延长[KA6h组3个亚组分别为(1879±827)s、(1907±569)s和(1065±227)s]、性发作次数明显少[KA6h组3个亚组分别为(1771±907)、(1865±1540)和(4525±1412)次]、平均振幅明显减小[KA6h组3个亚组分别为(458±126)μV、(431±135)μV和(752±289)μV],各项脑电指标的差异均有统计学意义(P<0.01)。CAR和CMP组之间脑电活动指标差异无统计学意义。致初期,CAR对脑电活动的相对抑制效果强于CMP,但从KA注射第3天开始,脑电活动的各项指标值相互接近,甚至CMP的各项指标超出CAR,但两组间差异无统计学意义。结论缝隙连接在癫发病中占有重要地位,CMP作为缝隙连接抑制剂可望成为治疗癫的新途径。
Objective To investigate the inhibitory effect of gap junction inhibitors on the electroencephalogram (EEG) activity of kainic acid (KA) -induced animal models. Methods The electrophysiological methods were used to observe the inhibitory effect of connexin mimetic (CMP) and carbenicillin (CAR) on the cortical EEG in different time periods after KA. Results Compared with the saline group, both CMP and CAR significantly prolonged the latency period (1879 ± 827 s, 1907 ± 569 s, and 1065 ± 227 s, respectively) in the three subgroups of KA6h group, (KA6h group, 3 subgroups were (1771 ± 907), (1865 ± 1540) and (4525 ± 1412) times, respectively), and the average amplitude was significantly decreased [456 ± 126 ) μV, (431 ± 135) μV and (752 ± 289) μV]. The differences of EEG indices were statistically significant (P <0.01). There was no significant difference in EEG parameters between CAR and CMP groups. In the early period of CAR, the relative inhibitory effect of CAR on EEG was stronger than that of CMP, but from the third day after KA injection, the values of EEG were close to each other, and even the indexes of CMP exceeded CAR, The difference was not statistically significant. Conclusion The gap junction plays an important role in the pathogenesis of epilepsy. CMP as a gap junction inhibitor is expected to become a new approach for the treatment of epilepsy.