Effect of acute stress on the expression of hypothalamic messenger ribonucleic acids encoding the endogenous opioid precursors preproenkephalin A and proopiomelanocortin.

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.