Epilepsy is associated with specific morphological and functional alterations in the hippocampus. There is growing evidence that functional alterations in epileptic hippocampus critically depend on GABAergic mechanisms and cation-chloride cotransporters. To elucidate changes in chloride homeostasis in epileptic tissue we studied the physiological characteristics and transmembrane currents of the cells in 350 mm thick slices of hippocampus from epileptic and control rats using whole-cell and gramicidin perforated patch clamp recordings. Whereas the resting membrane potential, input resistance, time constant, rheobase and chronaxy were not significantly different between two groups, the reversal potential of the GABA_AR mediated currents (E_GABA) was significantly shifted to more positive values in the epileptic rats. Western blot and pharmacological experiments showed the functional involvement of the main cation chloride cotransporters: the Na⁺-K⁺-2Cl^- cotransporter (NKCC1, Cl^--uptake) and the K⁺-Cl^- cotransporter (KCC2, Cl^--extrusion) in the observed changes.