Prolonged depolarization in the hippocampal CA1 region evokes a train of action potentials followed by an afterhyperpolarizing potential (AHP). Here, we studied the effect of acute epileptiform discharges induced by bath application of the GABA_A receptor blocker gabazine on the AHP. Therefore, we impaled CA1 pyramidal neurons to assess firing properties and to quantify the AHP under baseline conditions. Then gabazine was applied, and after 10–15 minutes the slices started to exhibit spontaneous epileptiform discharges monitored by an extracellular recording electrode. Prolonged depolarization (600 ms) elicited a train of action potentials, the number of which did not differ between baseline and gabazine treatment. However, the AHP following the train of action potentials was significantly reduced after gabazine treatment. In contrast, when the glutamate receptor blockers D-AP5 and CNQX were co-applied with gabazine in order to prevent the induction of epileptiform discharges, the AHP remained unaltered indicating that the gabazine-induced AHP reduction was due to the epileptiform discharges and not related to a direct action of the GABA_A receptor blocker. Moreover, the protein kinase inhibitors H-9 and H-89 could also prevent the gabazine-induced AHP reduction. These results demonstrate that the AHP following a train of action potentials is modulated by acutely induced epileptiform discharges. This AHP reduction in an acute model of epilepsy appears to be mediated by a phosphorylation process.