大鼠全脑缺血后海马CA1区锥体神经元L型钙通道电流的改变(英)

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15 min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.

Changes in Single L-Type Calcium Channel Currents in CA1 Pyramidal Neurons of Rat Hippocampus After Transient Forebrain Ischemia

It has been shown that intracellular Ca²⁺ in hippocampal CA1 neurons is elevated during ischemia and at early period following reperfusion. This Ca²⁺ overload has been suggested to be involved in ischemic brain damage. In normal CA1 neurons, the major mechanism allowing Ca²⁺ entry from the extracellular compartment is the opening of voltage-gated Ca²⁺ channels. The aim of the present study was to explore whether L-type calcium channel in hippocampal CA1 neurons changed at early period of reperfusion after ischemia. Transient forebrain ischemia in a duration of 15 min was induced by the use of the 4-vessel occlusion method in rats. Single L-type calcium currents were recorded in cell-attached patches of actually dissociated hippocampal CA1 neurons. After ischemia, average total patch current of L-type Ca²⁺ channels significantly increased in CA1 neurons when compared with that of control. This ischemia-induced enhancement in channel function was due to a higher channel open probability. Further analysis of single channel kinetics showed a prolonged open time and an increased opening frequency in postischemic channels. It is suggested that the functional enhancement in L-type calcium channels may partially account for the postischemic increase in intracellular Ca²⁺ concentration of CA1 neurons following ischemia.