Stress-induced release of brain and pituitary beta-endorphin: major role of endorphins in generation of hyperthermia, not analgesia.

The present paper examines the conjectured causal relationship between the alterations in brain, pituitary and plasma levels of endorphins and the antinociception (analgesia) and hyperthermia elicited by acute stress. A 5-min foot-shock instigated a significant depression in the levels of beta-endorphin immunoreactivity (beta-EI) in both the hypothalamus and periventricular beta-endorphinergic fibre-containing tissue. A large elevation in plasma levels of beta-EI, consisting of about 70% beta-endorphin (beta-EP), and 30% beta-lipotropin (beta-LPH) was associated with a significant reduction in the beta-EI content of both the anterior (AL) and neurointermediate (NIL) lobes of the pituitary. No concomitant changes in the levels of Met-enkephalin immunoreactivity (M-EI) in discrete areas of brain and pituitary were detectable. Application of a high (10 mg/kg) but not a low (1 mg/kg) dose of naloxone, prior to foot-shock, slightly reduced the increase in tail-flick latency evoked by this stress. In contrast, both of these doses strongly and dose-dependently attenuated the accompanying rise in core temperature (Tc). Chronic (approximately 30 day) morphine treatment resulted in a 45% decrease in the NIL content of beta-EI and a clear depression in its basal plasma levels, although a substantial post-stress rise in plasma beta-EI was still found: stress-induced analgesia (SIA) was enhanced, but the concurrent stress-induced hyperthermia (SIH), reduced in morphinized animals. These data demonstrate that stress produces a generalized mobilization of both central and pituitary pools of beta-EI, and indicate that endorphins may play a more important role in the mediation of changes in Tc than in the generation of the concomitant increase in nociceptive threshold, upon activation by stress.