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 IA in CA1 neurons shifted to the depolarizing direction at 38 h after ischemia. In granule cells, the amplitude and rising slope of IA were significantly increased at 38 h after ischemia; the inactivation curves of IA shifted toward the depolarizing direction accordingly at 38 h after ischemia. The IA 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 IKd 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 IA in dentate granule cells might have protective effects. The increase of IKd in CA1 neurons might be associated with the neuronal damage after ischemia.
- Cell death
- Cerebral ischemia
- Voltage dependent potassium currents
ASJC Scopus subject areas