短暂脑缺血大鼠海马CA1区锥体细胞大电导Ca2+依赖K+通道活动降低 |
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引用本文: | 胡平,李晓明,李建国,王颖,黄巧冰,高天明.短暂脑缺血大鼠海马CA1区锥体细胞大电导Ca2+依赖K+通道活动降低[J].生物化学与生物物理进展,2002,29(5). |
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作者姓名: | 胡平 李晓明 李建国 王颖 黄巧冰 高天明 |
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作者单位: | 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 |
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基金项目: | 国家自然科学基金,军队杰出人才基金,广东省自然科学基金,广东省自然科学基金 |
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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3 min短暂脑缺血后6 h、24 h以及48 h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24 h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.结果提示短暂脑缺血所致的BKCa通道活动降低可能与缺血耐受的产生有关.
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关 键 词: | 钾通道 短暂脑缺血 海马 膜片钳 大鼠 |
Brief Ischemia Decreases Large Conductance Ca2+-activated K+ Channel Activity in CA1 Pyramidal Neurons From Rat Hippocampus |
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Abstract: | 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. |
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Keywords: | K+ channel brief ischemia hippocampus patch clamp rat |
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