Aims: GABAergic transmission plays an important role in the initiation of epileptic activity and the generation of ictal discharges. The functional alterations in the epileptiform hippocampus critically depend on GABAergic mechanisms and cation-chloride cotransporters. Methods: To understand the cellular basis of specific morphological and functional alterations in the epileptic hippocampus we studied the physiological characteristics and pharmacologically isolated GABAergic transmembrane currents of neurones in hippocampal slices from epileptic and control rats using whole-cell and gramicidin perforated patch-clamp recordings. Results: Whereas the resting membrane potential, input resistance, time constant, rheobase and chronaxy were not significantly different between control and epileptic tissue, the reversal potential of GABA_AR mediated currents (E _GABA) was significantly shifted to more positive values in the epileptic rats and indeed beyond resting membrane potential (E _GABA: -76.2±1.9 mV (control rats) vs. -66.7±0.8 mV (epileptic rats) in DG and -75.3±2.0 mV (control rats) vs. -65.3±1.7 mV (epileptic rats) in Subiculum). Pharmacological experiments showed that the observed changes in the epileptic tissue were due to a combined upregulation of the main Cl^-- uptake transporter (NKCC1) and downregulation of the main Cl^-- extrusion transporter (KCC2). Conclusion: Our results suggest that alterations of cation chloride cotransporter functions, comprising a higher NKCC1 and a lower KCC2 action, may contribute to hyperexcitability and abnormal synchronisation within the epileptic hippocampus.