CA1 pyramidal neurons in the hippocampus die 2-3 days following transient forebrain
ischemia, whereas CA3 pyramidal neurons and granule cells in the dentate gyrus remain viable. Excitotoxicity is the major cause of ischemic cell death, and
potassium currents play important roles in regulating the neuronal excitability. The present study compared the changes of
potassium currents in acutely dissociated hippocampal neurons at different intervals after
ischemia. In CA1 neurons, the amplitude of rapid inactivating
potassium currents (I(A)) was significantly increased at 14 h and returned to control levels at 38 h after
ischemia; the rising slope and decay time constant of I(A) were accordingly increased after
ischemia. The activation curve of I(A) in CA1 neurons shifted to the depolarizing direction at 38 h after
ischemia. In granule cells, the amplitude and rising slope of I(A) were significantly increased at 38 h after
ischemia; the inactivation curves of I(A) shifted toward the depolarizing direction accordingly at 38 h after
ischemia. The I(A) remained unchanged in CA3 neurons after
ischemia. The amplitudes of delayed rectifier
potassium currents (I(Kd)) in CA1 neurons were progressively increased after
ischemia. No significant difference in I(Kd) was detected in CA3 and granule cells at any time points after reperfusion. These results indicated that the voltage dependent
potassium currents in hippocampal neurons were differentially altered after
cerebral ischemia. The up-regulation of I(A) in dentate granule cells might have protective effects. The increase of I(Kd) in CA1 neurons might be associated with the neuronal damage after
ischemia.