Evidence for the independence of brainstem mechanisms mediating analgesia induced by morphine and two forms of stress.

Exposure to inescapable footshock stress causes potent analgesia in the rat. According to several criteria, prolonged, intermittent footshock elicits analgesia mediated by opioid peptides, whereas brief, continuous footshock produces non-opioid analgesia. We now report that these neurochemically discrete forms of stress analgesia also have different neuroanatomical bases. Electrolytic lesions damaging greater than 85% of the n. raphe magnus ('complete' NRM lesions), but not lesions of the same size causing less NRM damage (partial NRM lesions) significantly reduce only the non-opioid form of stress analgesia. In the same animals, complete and partial NRM lesions disrupt morphine analgesia; however, our analyses indicate that this effect is not mediated by the same substrate involved in either form of stress analgesia. These results support the existence of multiple endogenous analgesia mechanisms and indicate a complex role for the NRM in these systems.