Pregnant rats were given diets containing either 5% ethanol, an isocaloric (pair-fed) diet, or casein pellets. Offspring were tested at postnatal day 10 for isolation-induced ultrasonic vocalizations and subsequent stress-induced analgesia. Rats prenatally exposed to ethanol vocalized significantly less in the five minutes during isolation. The opiate, morphine, caused a greater suppression of vocalizations in alcohol-exposed pups compared to controls, while the increased calling normally seen with the opiate antagonist, naltrexone, was attenuated. In a test in which the pup withdraws a paw from a hot plate (48 degrees C), prenatal alcohol offspring demonstrated baseline latencies (no isolation) similar to controls but had greatly attenuated responses in their isolation-induced analgesia. Since both vocalization and analgesia responses have been determined to be modulated by the endogenous opioid system, the aberrant responses of the prenatal-ethanol-exposed offspring can be interpreted as failures to respond by opioid release/secretion to appropriate stimuli.