短暂脑缺血大鼠海马CA1区锥体细胞大电导Ca^(2+)依赖K^+通道活动降低(英文)  

Brief Ischemia Decreases Large Conductance Ca^( 2+)-activated K^+ Channel Activity in CA1 Pyramidal Neurons From Rat Hippocampus

作　　者：胡平[1] 李晓明[1] 李建国[1] 王颖[1] 黄巧冰[2] 高天明[1] 

机构地区：[1]第一军医大学生理学教研室,广州510515 [2]第一军医大学病理生理教研室,广州510515

出　　处：《生物化学与生物物理进展》2002年第5期714-718,共5页Progress In Biochemistry and Biophysics

基　　金：国家自然科学基金 (3 9970 2 65 ;3 0 12 5 0 13 ) ;军队杰出青年基金 (0 1J0 0 9) ;广东省自然科学基金团队项目 (10 717);广东省自然科学基金 (990 3 95 )资助项目~~

摘　　要：短暂脑缺血可对随后的损伤性脑缺血表现出明显的耐受 .有研究表明大电导Ca2 + 依赖K+ (BKCa)通道活动增强参与了缺血性脑损伤 .采用膜片钳的内面向外式 ,观察了 3min短暂脑缺血后 6h、 2 4h以及 4 8h大鼠海马CA1区锥体细胞上BKCa通道活动的动态变化 .短暂脑缺血后BKCa通道的单通道电导和翻转电位均未见明显变化 ,但通道的开放概率则在缺血预处理后的前 2 4h内显著降低 .通道动力学分析显示通道关闭时间变长是短暂脑缺血后通道活动降低的主要原因 ,因为通道的开放时间未发生明显变化 .Preconditioning of the brain with brief ischamia induces tolerance to subsequent lethal periods of ischemia. It has been suggested that the enhancement in large conductance Ca2+-activated potassium (BKCa) channel activity is involved in the pathogenesis of ischemic neuronal injury. Inside-out configuration of patch clamp techniques were used to investigate the temporal changes in BKCa channel activity in CA1 pyramidal neurons acutely dissociated from rat hippocampus at 6 h, 24 h and 48 h following 3 min of brief ischemia. There were no changes in channel unitary conductance and reversal potential after brief ischemia. In contrast, a significant decrease in the channel open probability was observed during the first 24 h following brief ischemia. Kinetic analyses showed that the postischemic suppression of BKCa channel activity was due to a prolongation of the closed time since there was no significant change in open time after brief ischemia. It is suggested that the brief ischemia-induced suppression of BKCa channel activity may be associated with ischemic tolerance.

关 键 词：短暂脑缺血 大鼠 海马 CA1区 锥体细胞 大电导Ca^2+依赖K^+ 通道 膜片钳 

分 类 号：R743.31[医药卫生—神经病学与精神病学]