In neostriatal slices pretreated with sodium pentobarbital (100 microM) and 4-aminopyridine (50 microM), intrastriatal stimulation elicited EPSPs followed by a slowly decaying depolarization which lasted about 200 ms and was associated with a membrane conductance increase and a suppression of spike potentials. This depolarizing inhibitory synaptic action could be blocked by picrotoxin (50 microM) or bicuculline (50 microM). The reversal potential for the slowly decaying depolarization was -57 to -62 mV, i.e. it was positive with respect to the resting membrane potential (mean = -67 mV). GABA, injected into the tissue in the vicinity of the recording electrode by pressure application, or added to the perfusate (10 microM -1 mM), depolarized the cells and reduced both the membrane resistance and the amplitude of EPSPs. The reversal potential of GABA depolarization was found in a potential range approximating that of the slowing decaying depolarization. These results are compatible with the assumption that GABA is the transmitter of an intrinsic inhibition in rat neostriatum, but indicate that GABA-mediated IPSPs of neostriatal cells in vitro are depolarizing at the resting membrane potential. The possible reasons for this are discussed.