After-hyperpolarizing currents following action potentials play a major role in controlling neuronal excitability which is severely altered in epileptic brain tissue. Therefore, we used the patch- clamp technique to study isolated CA1 pyramidal neurons of chronically epileptic rats after pilocarpine-induced status epilepticus. While not differing in cell morphology, resting membrane potential, whole-cell capacitance, spike amplitude and spike frequency upon long-lasting depolarizing current injection, neurons of epileptic rats exhibited significant spike broadening. Moreover, the after-hyperpolarization following the spike train was significantly decreased suggesting impaired Ca2+ -activated K+ currents. When voltage-dependent Na+ and K+ currents were blocked by TTX and tetraethylammonium, depolarizing current injection caused an outward tail current in control neurons that was at least partially sensitive to the small-conductance Ca2+ - activated K+ channel (SK) blocker apamin. In neurons from epileptic rats, however, the outward tail current was significantly reduced and apamin had virtually no effect suggesting alterations of SK channel expression or gating in chronic epileptic rats.