Analgesia induced by painful stimulation and/or anticipation of pain; different mechanisms are operating.

Various stresses (i.e. transfer stress, exposition of animals to a new environment, footshock stress, anticipation stress) were found to produce hypalgesia as judged from an increase of the tail - flick latency in rats. Hypalgesia induced by transfer stress was slightly reduced by diazepam (5 mg per kg), but very significantly by chlorpromazine (5 mg per kg). Footshock-stress-induced analgesia lasted less than 15 min. Because naloxone or dexamethasone did not block the footshock-induced analgesia, the participation of the endorphinergic system in this form of stress-induced analgesia is not probable. During the 30 min lasting conditioned reaction to footshock administration (called here anticipation stress), marked analgesia was observed. This anticipation-stress-induced analgesia was blocked by naloxone, dexamethasone and chlorpromazine; no blockade was observed after diazepam. These observations suggest that the endorphinergic system in this form plays a role in stress-induced analgesia. The comparison of the effects of naloxone and/or dexamethasone on the analgesia induced by footshock on the one hand and analgesia induced by anticipation stress on the other thus suggests that different antinociceptive mechanisms are activated by the unconditioned and/or conditioned stimulus.