The aim of the study was to determine the role of dopamine on the GABAergic input to striatal projection neurons. Accordingly, the effect of the activation of dopamine D2-like receptors on GABA-mediated depolarizing postsynaptic potentials evoked in striatal slices by local stimulation was studied. Conventional intracellular recording techniques were used to record the synaptic responses. The experiments were done in the presence of 6-cyano-7-nitroquinoxaline-2,3-dione (20 microM) and (+)-2-amino-5-phosphonovaleric acid (40 microM) to block the participation of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate/kainate and N-methyl-D-aspartate receptors in the synaptic response. The GABAergic nature of the response was assessed by its potentiation by pentobarbital (50 microM) and by its elimination by bicuculline or picrotoxin. At 100 nM, a concentration already maximal, dopamine inhibited by 55% the GABAergic synaptic response. The inhibitory effect was totally blocked by the selective antagonist of D2-like receptors, sulpiride (100 nM). The dopamine inhibition was observed only in one-third of the studied neurons and was concentration dependent (IC50 = 14 nM). The inhibition was not associated with changes in the input resistance or any other membrane property. In addition, dopamine (50 nM) reduced the frequency but not the amplitude of spontaneous, bicuculline-sensitive depolarizing postsynaptic potentials. The D2-like receptor agonist quinpirole also dose-dependently (IC50 = 10 nM) inhibited the GABAergic synaptic response. As with dopamine, the inhibition did not change the membrane properties of the studied neurons. In addition, the quinpirole induced inhibition of the GABA response was accompanied by increased paired-pulse facilitation. The results indicate that D2-like receptors located on intrinsic GABAergic terminals in the rat striatum exert an inhibitory control of the GABAergic input to striatal projection neurons. The dopaminergic effect would be translated in facilitation of the firing of the neurons upon the arrival of the cortical input.