Correlation between magnitude and opioid mediation of stress-induced analgesia: individual differences and the effect of selective breeding.

Two experiments were made showing that opioid involvement coincides with the magnitude of stress-induced analgesia. In Experiment I rats subjected to cold water swims were screened for jump threshold levels on electrified grid and divided into high, medium and low threshold responders' groups. Later on the three groups were given 90 s forepaw footshock. Tail-flick latencies rose highest in the high threshold, and lowest in the low threshold responders. This decrease in nociception was counteracted by naloxone more effectively in high than in medium threshold responders, and not all in low threshold responders. In Experiment II mice selectively bred for high (HA) and low (LA) post-stress analgesia swam at 20 and 2 degrees C. Both stressors were followed by an increase in tail-flick latencies in the order of magnitude HA greater than unselected controls greater than LA line. Naloxone attenuated analgesia after both stressors in the HA line, but was ineffective in LA mice. In unselected controls swimming at 20 degrees C caused naloxone-sensitive, and cold water swims naloxone-resistant analgesia. It is concluded that apart from the kind of stressor, inborn properties of an individual are essential for the development of opioid vs. non-opioid form of post-stress analgesia.