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Query: UMLS:C0848237 (acute stress)
 4,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:Stress-induced release of brain and pituitary beta-endorphin: major role of endorphins in generation of hyperthermia, not analgesia. 626 Feb 87

In addition to the release of adenohypophysial hormones adrenocorticotropin and beta-endorphin, most types of acute stress induce rapid release of prolactin (PRL) from the anterior pituitary lobe. Endogenous opioid peptides are believed to participate in the stress-induced PRL secretion via an action within the central nervous system. In the present study, we have investigated the effect of acute stress on anterior pituitary PRL secretion and the hypothalamic expression of messenger ribonucleic acids (mRNAs) encoding precursors of the endogenous opioids Met-enkephalin and beta-endorphin. Adult male rats were subjected to 1 h of restraint and the stress-induced rise in plasma PRL was measured both during and after termination of the stress paradigm. Using quantitative in situ hybridization histochemistry, it was observed that levels of proenkephalin A mRNA increased significantly within the medial parvocellular subset of the hypothalamic paraventricular nucleus, and within the arcuate nucleus levels of proopiomelanocortin (POMC) mRNA were slightly, but significantly, increased. The employed stress paradigm also induced an elevation of anterior pituitary levels of PRL and POMC mRNAs. The present data suggest that restraint stress activates gene expression of endogenous opioid systems in the hypothalamus and that the employed stress paradigm is of sufficient magnitude to stimulate both mRNA expression and release of PRL in the anterior pituitary lobe.
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PMID:Effect of acute stress on the expression of hypothalamic messenger ribonucleic acids encoding the endogenous opioid precursors preproenkephalin A and proopiomelanocortin. 798 95