Possible Involvement of Endogenous Opioid Peptides in Prolactin Secretion Induced by α 2 -Adrenergic Stimulation in Rats

Abstract

Noradrenergic mechanisms have a stimulatory role in regulating prolactin (PRL) secretion in the rat. We investigated the mechanism by which the α ₂-adrenergic system stimulates PRL release in urethane-anesthetized male rats. Intracerebroventricular injection of norepinephrine (2 μg/rat) or epinephrine (100 ng and 1 μg/rat) caused an increase in plasma PRL levels. The PRL increase induced by epinephrine was much greater than that by norepinephrine. Intracerebroventricular injection of phentolamine (1 μg/rat), an α-antagonist, blunted the plasma PRL increase induced by epinephrine (100 ng intracerebroventricularly). Plasma PRL levels were increased by intravenous injection of α ₂-agonists, clonidine (15 μg/100 g of body wt), and xylazine (200 μg/100 g of body wt). Plasma PRL increase induced by clonidine or xylazine was suppressed by intravenous injection of naloxone (125 μg/100 g of body wt), an opiate antagonist. These findings suggest that α ₂-adrenergic mechanisms stimulate pituitary PRL secretion, at least partly, by activating endogenous opioid peptides in the rat.