短暂脑缺血对大鼠海马脑区锥体神经元外向整流氯通道功能的影响  

The Influence of Transient Forebrain Ischemia on the Outwardly Rectifying Chloride Channels in Pyramidal Neurons of Rat Hippocampus

作　　者：李建国[1] 刘乃红[1] 陈建鸣[1] 

机构地区：[1]山西医科大学

出　　处：《中西医结合心脑血管病杂志》2012年第2期209-211,共3页Chinese Journal of Integrative Medicine on Cardio-Cerebrovascular Disease

摘　　要：目的研究短暂前脑缺血对大鼠海马CA1和CA3脑区锥体神经元外向整流氯通道功能的影响。方法采用膜片钳全细胞技术,在成年大鼠海马脑区锥体神经元上记录到可以被氯通道阻断剂DIDS阻断,具有外向整流特性的氯通道。结果 15min前脑缺血再灌注6h和24h后,海马CA1区锥体神经元氯通道电流持续性增强,而CA3区锥体神经元活动无明显改变。结论氯通道功能增强可能参与海马CA1区锥体神经元在脑缺血后的迟发性死亡过程,并且为治疗缺血性脑损伤提供了新的手段。Objective To investigate the effect of transient forebrain ischemia on the outwardly rectifying chloride channels（ORCC） in pyramidal neurons of rat hippocampus.Methods The ORCC currents were studied by whole-cell patch-clamp technique,which one kind of chloride channel blocker 4,4＇-diisothiocyanatostilbene-2,2＇-disulfonic acid（DIDS） could be blocked.Results After 6 hours and 24 hours reperfusion after 15 min forebrain ischemia,ORCC activity in CA1 and CA3 pyramidal neurons of rat hippocampus were examined.ORCC activity was persistently unregulated in vulnerable CA1 neurons after ischemic insult,whereas no change occurred in invulnerable CA3 neurons.Conclusion The present results suggest that the enhanced activities of ORCC may contribute to the selective neuronal damage in vulnerable CA1 region after transient forebrain ischemia,and ORCC would be a therapeutic target against the ischemia-induced neuronal damage.

关 键 词：外向整流氯通道 膜片钳 脑缺血 神经元死亡 海马 

分 类 号：R743[医药卫生—神经病学与精神病学] R255.2[医药卫生—临床医学]