The uptake of the inhibitory transmitter GABA (gamma-aminobutyric acid) limits the efficacy of synaptic and tonic inhibition in brain tissue. It has been reported that GABA-uptake is down-regulated in temporal lobe epilepsy. This down-regulation may increase the inhibitory action of GABA but may also limit the anticonvulsant activity of GABA-uptake blockers. We have directly compared the function of GABA-uptake in hippocampal slices from normal and chronically epileptic rats. We raised the global extracellular concentration of GABA by bath-application of the agonist in the absence and presence of the GABA-uptake blocker tiagabine. GABA-induced currents were measured in dentate granule cells and CA1 pyramidal neurons in hippocampal slices. The potentiation of currents by tiagabine was taken as a measure for the efficacy of GABA-uptake in the hippocampal tissue. There was no difference between cells from control- or pilocarpine-treated animals in the response to GABA or in the conductance increase following application of tiagabine. Our data show that in the chronic phase of the pilocarpine-model GABA-uptake maintains its ability to control the extracellular background concentration of GABA.