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 (BK_Ca) 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 BK_Ca 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 BK_Ca 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 BK_Ca channel activity may be associated with ischemic tolerance.