无镁诱导海马神经元癫痫样放电中Cx32作用的研究  

Involvement of connexin 32 in epileptiform discharges induced by zero-Mg^(2+) in cultured hippocampal neurons in rat

作　　者：赵秀鹤[1] 迟兆富[1] 迟令懿[1] 尚伟[2] 刘学伍[1] 

机构地区：[1]山东大学齐鲁医院神经内科,山东济南250012 [2]山东大学第二医院神经内科,山东济南250033

出　　处：《山东大学学报（医学版）》2006年第1期36-40,共5页Journal of Shandong University:Health Sciences

摘　　要：目的:探讨缝隙连接在癫痫发病机制中的作用。方法:采用无镁液诱导的体外原代培养新生大鼠海马神经元细胞癫痫模型,应用膜片钳技术记录细胞外放电。观察放电不同时点缝隙连接蛋白Cx32的表达情况,以及生胃酮和卡马西平的抑制作用。结果:神经元经无镁培养液处理3h后产生稳定的放电,放电后Cx32表达显著增多,8h后可达对照组5倍。生胃酮和卡马西平均可抑制神经元的放电。生胃酮显著抑制了Cx32的表达,而卡马西平组Cx32水平无明显变化。结论:缝隙连接参与癫痫的发生发展过程,而且具有独立于传统的化学性突触的机制,为开发新的作用于缝隙连接的治疗药物提供了思路。Objective： To study the role of gap junction in epileptiform activity induced by zeroMg^2＋ in cultured hippocampal neurons in rats. Methods： The epileptiform activity following zero-Mg^2＋ medium in cultured neurons for 3 hours was recorded with whole-cell patch clamp recording techniques. Besides the expression of Cx32 protein of neurons at different time after discharging, the inhibition by carbenoxolone and carbamazepine was determined. Results： During the zero- Mg^2＋ medium exposure, regular seizure-like discharges developed at 3 hours in neurons. The expression level of Cx32 protein began to develop at 2 hours after restoration to normal medium and was raised by five times at 8 hours compared to the results from the control group. Both carbenoxolone and carbamazepine could inhibit the interictal-like activily, however only carbenoxolone depressed the expression of Cx32 to the level in control group and carbamazepine showed little effect on Cx32. Conclusions： Gap junction contributes to epileptiform activity with different mechanismswith the traditional chemical synapse, suggesting a direction for the development of new drugs targeting gap junctions for therapeutic intervention.

关 键 词：缝隙连接 癫痫 细胞培养 生胃酮 卡马西平 

分 类 号：R741.02[医药卫生—神经病学与精神病学]