Changes in Single L-Type Calcium Channel Current, 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 CAI 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 CAI neurons. After ischemia, average total patch current of L-type Ca2+ channels significantly increased in CAI 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.
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