Rabbits were treated intravenously with either naloxone-HCl (0.5 mg/kg) or saline vehicle prior to aversive pavlovian conditioning and extinction training; heart rate conditioned responses and concomitant multiple-unit activity in the amygdaloid central nucleus were compared. Multiple-unit activity evoked by the conditioned stimulus increased during conditioning and decreased during extinction in saline-treated rabbits; naloxone treatment attenuated evoked neuronal activity but enhanced bradycardiac conditioned responses. Correlational analysis showed that, in 3 of 8 animals in the saline-treated group, larger increases in multiple-unit activity corresponded to smaller bradycardiac responses. Naloxone treatment did not alter the frequency or magnitude of this relationship, but it did augment the training-induced decrements in evoked neuronal activity at placements that were correlated with bradycardiac response magnitude. These data suggest that conditioned decreases in central nucleus neuronal activity normally may serve to disinhibit vagal mechanisms as conditioned bradycardia develops and that the neural circuits that produce these responses are sensitive to opioid modulation.