Objective: In the hippocampal CA1 region prolonged depolarisation evokes a train of action potentials followed by an afterhyperpolarising potential (AHP). Here, the effect of GABA_A receptor inhibition by gabazine on the AHP was investigated. Methods: Conventional extracellular recordings were performed to monitor the wash-in of gabazine leading to spontaneous epileptiform discharges in the slice. Additionally, CA1 pyramidal neurons were impaled to measure basic cell characteristics and intrinsic firing properties. Results: Following 10-15 minutes of gabazine wash-in, slices started to exhibit spontaneous epileptiform discharges. This was accompanied by a shift of the resting membrane potential to more positive values and an increase of the input resistance of the CA1 pyramidal neurons. Other properties like the membrane time constant, the action potential threshold or action potential shape were not changed after gabazine. Prolonged depolarisation (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. Conclusion: These results demonstrate that the AHP following a train of action potentials is modulated by GABA_A receptor mediated signalling. Thus, we suggest that tonic inhibition by GABAergic interneurones facilitates the AHP after an action potential train.