the understanding of cellular and molecular aspects of dopaminergic and glutamatergic receptor interaction, little is known about the interaction between glutamatergic and dopaminergic function in the nAcb during postnatal development. Recent studies have shown that there are important changes in glutamatergic neurotransmission from the day of birth throughout adulthood. Of particular interest is a change in the amplitude of the NMDA receptor-mediated excitatory postsynaptic current to AMPA receptor-mediated EPSC ratio which reaches its maximum toward the end of the second postnatal week and decreases after that until adulthood. In addition to changes in glutamatergic neurotransmission, it has also been found that postnatal development is accompanied by changes in the dopaminergic innervation as well as the density and expression of dopaminergic receptors. The effects of dopamine on glutamatergic neurotransmission have been previously studied. Some studies reported that the activation of D1 receptors enhanced NMDA receptor-mediated EPSCs in dorsal striatal slices, while others reported that D1 receptor agonists attenuated NMDA EPSCs in MS striatal neurons in culture. In the nAcb, some investigators reported that DA or D1 receptor agonists potentiate NMDA receptor-mediated EPSCs in slices, while others reported no significant modulatory effects of DA on NMDA receptor-mediated EPSCs but the presynaptic inhibitory effect of DA on EPSCs was only determined on AMPA/KA receptormediated EPSCs in the nAcb. A substantial effect of DA on pharmacologically isolated NMDA and AMPA/KA receptormediated EPSCs remains to be determined. In a previous study, we showed that acetylcholine presynaptically modulated AMPA/KA and NMDA receptors mediated EPSCs in a parallel fashion in the nAcb during postnatal development. In an effort to clarify how the NMDA and AMPA/KA EPSCs might be affected in the nAcb by dopaminergic innervation, we investigated the effect of DA on NMDA and AMPA/KA excitatory synaptic transmission in this region. Our results demonstrate that DA depresses the excitatory input onto MS neurons by the activation of presynaptic D1-like receptors. While DA depressed the elicited AMPA/KA receptor-mediated EPSCs in MS neurons by 40% of the control, DA almost completely abolished NMDA receptor-mediated EPSC. The effects of DA on glutamatergic EPSCs remained constant throughout the first 3 postnatal weeks. We found that DA inhibited glutamatergic EPSCs in MS neurons recorded in an in vitro slice preparation. Whereas both AMPA/KA and NMDA receptors-mediated components of the EPSCs were significantly inhibited by DA, the inhibition of the NMDA receptor-mediated component was much more pronounced than that of the AMPA/KA receptor-mediated component. Pharmacological evidence suggests that dopaminergic inhibitory effects were mediated by the activation of presynaptic D1-like receptors and that D2-like receptors were not involved.