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 brainstem slices. ST-evoked EPSCs were significantly reduced by met-enkephalin (MetE) in a concentration dependent fashion, and this effect was eliminated by naltrexone hydrochloride (NTX), a non-selective opioid receptor antagonist. Bath application of naltrindole hydrochloride (NTD), a selective -opioid receptor antagonist, eliminated MetE-induced reduction of EPSCs while CTOP, a selective µopioid receptor antagonist had no effect, indicating that -opioid receptors are involved in the reduction of ST-evoked EPSCs induced by MetE. SNC80, a selective -opioid receptor agonist, mimicked the effect of MetE. The SNC80-induced reduction of ST-evoked EPSCs was eliminated by 7-benzylidenenaltrexone (BNTX), a selective 1-opioid receptor antagonist but not by neltriben mesylate (NTB), a selective 2-opioid receptor antagonist, indicating that 1-opioid receptors mediate the reduction of ST-evoked EPSCs induced by SNC80. Single-cell reverse transcriptase (RT)-PCR analysis revealed the presence of 1-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 -receptor proteins in the rostral NST tissue. These results suggest that postsynaptic 1-opioid receptors are involved in opioid-induced reduction of ST-evoked EPSCs of PbN-projecting rostral NST cells.