Influence of prolactin on dopaminergic neuronal systems in the hypothalamus

Abstract

The release of prolactin from the anterior pituitary is tonically inhibited by dopamine (DA), which is released from terminals of tuberoinfundibular neurons. These nerves, which originate in the mediobasal hypothalamus and terminate in the external layer of the median eminence, differ from other DA nerves in the brain in that they: 1)lack a high affinity DA uptake mechanism, 2) are not responsive to the acute administration of DA agonists or antagonists, 3) are responsive to increased concentrations of prolactin in blood or cerebrospinal fluid. The activity of different DA neuronal systems in the rat brain was estimated in terminals of these nerves by measuring: 1) the rate of decline of DA after the administration of a tyrosine hydroxylase inhibitor, alpha-methyltyrosine, or 2) the rate of accumulation of dopa after the administration of a decarboxylase inhibitor, NSD 1015. Systemic or intracerebroventricular injections of exogenous prolactin selectively increased the activity of tuberoinfundibular DA nerves. Furthermore, pharmacological manipulations that increased serum concentrations of endogenous prolactin (injections of DA antagonists or estrogen) also increased activity of tuberoinfundibular DA nerves. The prolactin-induced increases in tuberoinfundibular nerve activity were first noted 12-16 h after the prolactin concentrations increased. These results suggest that prolactin can exert a sluggish control over its own release by activating the tuberoinfundibular DA nerves that normally inhibit the release of this hormone.