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目的 研究缺氧对大鼠大脑皮层神经元钙激活性钾 (Kca)通道的影响 ,以揭示神经元抗缺血损伤的电生理机制。方法 在不同缺氧条件下 ,应用膜片钳技术记录大脑皮层神经元上Kca通道电流活动。电流信号经放大、滤波及A/D、D/A转换后输入微机进行采样和储存。实验数据应用PClamp(6 .0 .2 )软件进行分析处理。结果 缺氧对通道的开放概率 (Po)及平均开放时间 (To)有明显影响 ,在缺氧实验早期通道Po明显增加 ,其中 10 μmol·L-1NaCN缺氧组其增加程度大于 2 0 μmol·L-1和 30 μmol·L-1NaCN缺氧组 (P <0 .0 5 )。而在缺氧实验后期通道Po和To明显降低 ,其中 30 μmol·L-1NaCN缺氧组其降低程度大于 2 0 μmol·L-1和 10 μmol·L-1NaCN缺氧组 (P <0 .0 5 )。结论 缺氧早期大脑皮层神经元Kca通道激活 ,产生超极化电位 ,从而稳定细胞膜 ,降低细胞兴奋性 ,延缓缺氧除极的发生 ,这可能是神经元自身的一种代偿作用
Objective To investigate the effect of hypoxia on calcium-activated potassium channel (KCa) in rat cerebral cortex to reveal the electrophysiological mechanism of neuronal anti-ischemic injury. Methods Under different hypoxic conditions, patch clamp technique was used to record Kca channel current activity in cerebral cortical neurons. The current signal is amplified, filtered and A / D, D / A conversion input to the computer for sampling and storage. Experimental data using PClamp (6 .0 .2) software for analysis and processing. Results Hypoxia had a significant effect on the open probability (Po) and mean open time (To) of the channel, and Po significantly increased in the early phase of hypoxia. The increase of hypoxia in 10 μmol·L-1 NaCl was greater than 20 μmol · L-1 and 30 μmol·L-1NaCN hypoxia group (P <0.05). In the hypoxia experiment, the channel Po and To decreased obviously, and the degree of decrease in 30 μmol·L-1NaCN hypoxia group was greater than that in the hypoxia group of 20 μmol·L-1 and 10 μmol·L-1NaCN (P <0. 0 5). Conclusions Activation of Kca channel in the early stage of hypoxia leads to hyperpolarization potentials that stabilize the cell membrane and reduce the excitability of cells and delay the occurrence of hypoxia and depolarization, which may be a compensatory action of neurons themselves