【摘要】 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更多还原

【Abstract】 Objective To study the influence of hypoxia to the calcium activated potassium (K ca ) channels in cultured newborn rat corticocerebral neurons and to reveal the electronic physialogical mechanism of neurons in anti ischemic injury.Methods In different hypoxia conditions,K ca channal current was recorded with patch clamp technique in the corticocerebral neurons. Single channel current signals were enlarged and filtered by patch clamp amplifer(CEZ 200),then input to computer via A/D?D/A converter.Experimental datas were analysed using PCLamp software(Version 6.0.2 ).Results Hypoxia has great influence on the channels open probability(Po) and open time(To). At the first stage of the experiment,Po increases obviously and in the 10 μmol·L -1 NaCN hypoxia group it increases higher than in the 20 and 30 μmol·L -1 NaCN groups( P < 0.05 ). At the last stage of the experiement,Both Po and To reduces obviously and in the 30 μmol·L -1 NaCN group it reduces more than in the 20 and 10 μmol·L -1 NaCN groups( P < 0.05 ). Conclusions At the first stage of hypoxia, activation of the K ca channels induce cell membrane hyperpolarization against hypoxic depolarization,therefore stablize cell membrane and reduce cell excitability. This is probably the compensative mechanism of neurons.更多还原