Changes in hypothalamic preproenkephalin A mRNA following stress and opiate withdrawal

Abstract

The median eminence of the pituitary is rich in opioid receptors¹, and exogenous opioids have major effects on the release of adrenocorticotropic hormone (ACTH)^2,3, luteinizing hormone (LH)^4,5, prolactin^4,6, growth hormone (GH)^4,6 and thyrotropin^7,8. Stress results in similar changes in anterior pituitary hormone secretion. Enkephalin immunoreactivity has been reported in the medial parvocellular neurons of the hypothalamic paraventricular nucleus which project to the median eminence^9–12, the site where hypothalamic releasing factors are secreted into the portal blood and thence to the anterior pituitary gland. The endocrine response to stressful stimuli might therefore, at least in part, be mediated through the activation of hypothalamic enkephalinergic neurons. We show that two stressful stimuli, opiate withdrawal and intraperitoneal injection of hypertonic saline, both result in very rapid and marked increases in enkephalin mRNA in the parvocellular paraventricular nucleus. The activation of hypothalamic enkephalin neurons may be important in the neuroendocrine response to stress.