Brief ischemia decreases large conductance Ca2+-activated K+ channel activity in CA1 pyramidal neurons from rat hippocampus

Preconditioning of the brain with brief ischamia induces tolerance to subsequent lethal periods of ischemia. It has been suggested that the enhancement in large conductance Ca2+-activated potassium (BKCa) channel activity is involved in the pathogenesis of ischemic neuronal injury. Inside-out configuration of patch clamp techniques were used to investigate the temporal changes in BKCa channel activity in CA1 pyramidal neurons acutely dissociated from rat hippocampus at 6 h, 24 h and 48 h following 3 min of brief ischemia. There were no changes in channel unitary conductance and reversal potential after brief ischemia. In contrast, a significant decrease in the channel open probability was observed during the first 24 h following brief ischemia. Kinetic analyses showed that the postischemic suppression of BKCa channel activity was due to a prolongation of the closed time since there was no significant change in open time after brief ischemia. It is suggested that the brief ischemia-induced suppression of BKCa channel activity may be associated with ischemic tolerance.