The rostral nucleus of the solitary tract (NST) is the first central relay in the gustatory pathway and plays a key role in processing and modulation of gustatory information. Here, we investigated the effects of opioid receptor agonists and antagonists on synaptic responses of the gustatory parabrachial nuclei (PbN)-projecting neurons in the rostral NST to electrical stimulation of the solitary tract (ST) using whole cell recordings in the hamster brain stem slices. ST-evoked excitatory postsynaptic currents (EPSCs) were significantly reduced by met-enkephalin (MetE) in a concentration-dependent fashion and this effect was eliminated by naltrexone hydrochloride, a nonselective opioid receptor antagonist. Bath application of naltrindole hydrochloride, a selective delta-opioid receptor antagonist, eliminated MetE-induced reduction of EPSCs, whereas CTOP, a selective mu-opioid receptor antagonist had no effect, indicating that delta-opioid receptors are involved in the reduction of ST-evoked EPSCs induced by MetE. SNC80, a selective delta-opioid receptor agonist, mimicked the effect of MetE. The SNC80-induced reduction of ST-evoked EPSCs was eliminated by 7-benzylidenenaltrexone, a selective delta1-opioid receptor antagonist but not by naltriben mesylate, a selective delta2-opioid receptor antagonist, indicating that delta1-opioid receptors mediate the reduction of ST-evoked EPSCs induced by SNC80. Single-cell reverse transcriptase-polymerase chain reaction analysis revealed the presence of delta1-opioid receptor mRNA in cells that responded to SNC80 with a reduction in ST-evoked EPSCs. Moreover, Western blot analysis demonstrated the presence of 40-kDa delta-opioid receptor proteins in the rostral NST tissue. These results suggest that postsynaptic delta1-opioid receptors are involved in opioid-induced reduction of ST-evoked EPSCs of PbN-projecting rostral NST cells.