钙激活钾通道及ATP敏感性钾通道在海马神经元缺氧超极化中的作用

研究缺氧超极化缺氧海马神经元中的电生理机制，以提示缺氧超极化在脑损伤中的作用。方法：应用膜片钳制技术的细胞贴附式膜片记录缺氧海马神经元的单通道电流活动，经p-CLAMP软件进行采样储存数据和数据的分析处理。结果：缺氧引起钙激活钾通道（KCa通道）和ATP敏感性通道（KATP通道）的激活，增加通道的开放概率。结论：缺氧超极化可能是缺血性脑损伤早期的重要代偿机制。

CONTRIBUTION OF Ca~(2 ) - ACTIVATED POTASSIUM CHANNELS AND ATP - SENSITIVE POTASSIUM CHANNELS TO HYPOXIC HYPERPOL ARIZATION IN RAT HIPPOCAMPAL NEURONS

Objective: The electrophysiological mechanisms underlying hypoxic hyperpolarization of hippocampal neurons were studied to reveal the role of hypoxic hyperpolarization in brain injuries. Methods: Cell-attached configuration of patch clamp technique was used to record the activity of single channel, application of p-CLAMP software for data sampling, storing, and analysing. Results: Ca 2 - activated potassium channels (K Ca channels) and ATP - sensitive potassium channels (K ATP channels) could be activated by hypoxia which increased their open probability. Conclusion: Hypoxic hyperpolarization may be an adaptive mechanism that can protect neurons against cerebral ischemic injury in early hypoxic stage.