Recent evidence suggests that certain forms of opioid-mediated hypoalgesia may depend on monosynaptic projections from the amygdala to nociceptive modulatory neurons in the midbrain. We recently demonstrated that the microinjection of morphine sulfate into the basolateral nucleus of the amygdala will result in a robust elevation of radiant heat tail flick (TF) latency in the pentobarbital-anesthetized rat. The present study was conducted to begin to clarify the opioid receptor type(s) responsible for this effect. Rats were anesthetized with sodium pentobarbital and prepared for microinfusion and TF testing. Rats received simultaneous bilateral infusions of agonists for mu ([D-Ala2, N-MePhe4, Gly-ol 5] enkephaphalin (DAMGO); 0.01, 0.05, 0.1, 1.0 or 5.0 micrograms), delta ([D-Pen2, D-Pen5]enkephalin [DPDPE]; 6.458 or 64.58 micrograms) or kappa (trans-3,4-dichloro-N-methyl-N-(2-(1-pyrolidinyl)-cyclohexyl)-benz ene acetamide methanesulfonate hydrate [U50, 488H]; 5.0, 40.0 or 84.0 micrograms) opioid receptors during TF testing. The mu agonist produced a dose- and time-dependent elevation in TF latency when injected into the basolateral amygdala. Application of the delta and kappa agonists to similar sites within the amygdala was without effect. In separate experiments, U50, 488H and DPDPE were injected into the lateral ventricle at concentrations similar to those applied to the amygdala. Intracerebroventricular administration of these compounds resulted in reliable inhibition of TF. These results indicate that mu opioid receptors in the basolateral amygdala may be able to modulate transmission in a recently identified neural circuit that is at least partially responsible for the expression of stress-related hypoalgesia in behaving animals.