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已有研究表明在脑缺血期间及再灌流后早期,海马CA1锥体神经元细胞内钙浓度明显升高,这一钙超载被认为是缺血性脑损伤的重要机制之一.电压依赖性钙通道是介导正常CA1神经元钙内流的主要途径.实验观察了脑缺血再灌流后早期海马CA1锥体神经元电压依赖性L型钙通道的变化.以改良的四血管闭塞法制作大鼠 15min前脑缺血模型,在急性分离的海马CA1神经元上,采用膜片钳细胞贴附式记录L型电压依赖性钙通道电流.脑缺血后CA1神经元L型钙通道的总体平均电流明显增大,这是由于通道的开放概率增加所致.进一步分析单通道动力学显示,脑缺血后通道的开放时间变长,通道的开放频率增大.研究结果提示L型钙通道功能活动增强可能参与了缺血后海马CA1锥体神经元的细胞内钙浓度升高
It has been reported that during cerebral ischemia and early after reperfusion, the intracellular calcium concentration in hippocampal CA1 pyramidal neurons is significantly increased, and this calcium overload is considered as one of the important mechanisms of ischemic brain injury.Voltage-dependent Calcium channel is the main pathway to mediate calcium influx in normal CA1 neurons.The changes of voltage-dependent L-type calcium channel in hippocampal CA1 pyramidal neurons after cerebral ischemia and reperfusion in rats were observed.An improved four vessel occlusion method In 15 min forebrain ischemia model, voltage-dependent calcium channel current was recorded by patch clamp in acutely isolated hippocampal CA1 neurons.After cerebral ischemia, the total number of L-type calcium channels in CA1 neurons The average current significantly increased due to the increase of the open probability of the channel.Further analysis of the single channel kinetics showed that the opening time of the channel became longer and the channel open frequency increased after cerebral ischemia.The results suggest that L-type calcium channel Increased functional activity may be involved in increased intracellular calcium concentration in hippocampal CA1 pyramidal neurons after ischemia