Recent evidence indicates a close connection between oral sensory function and opioid effects on feeding. Not only is gustatory motivation influenced by opiate drugs [11] but apparently gustatory stimuli can also activate central opiate receptor systems [3]. In 3 experiments we studied the effect of opiate receptor blockade on drinking motivated by the sweet taste of saccharin. Experiment 1 established a dose-response function for inhibition of intake by naloxone (NAL) in short (60 min) 2-bottle tests. This experiment demonstrated the extreme sensitivity of nondeprived, nonstressed animals to NAL and estimated the MED 50 at less than 0.1 mg/kg (SC), well below the threshold for effects due to illness or general motor disturbance. Experiment 2 further demonstrated that NAL's effectiveness depends on saccharin concentration. In particular, the lowest NAL dose studied was effective near the threshold for saccharin preference but not at higher concentrations. These data suggest that endogenous opioid systems may be activated by taste stimuli in a graded fashion. Finally, experiment 3 showed that the typical acquisition of preference for a moderate saccharin concentration can be effectively blocked by daily pre-test NAL injection. Together these experiments further demonstrate the close functional relationship between opioid systems and gustatory sensory systems.