Effects of prolactin and ergot alkaloids on the tubero-infundibular dopamine (DA) neurons.

Abstract

Using the Falck-Hillarp fluorescence technique, the effect of various hypophyseal hormones on the rate of depletion of catecholamines (CA) from certain central neuron systems was investigated in the rat, after inhibition of CA synthesis. Prolactin, but not LH, FSH, ACTH, or vasopressin, caused a dose-dependent increase in the turnover of dopamine (DA) in nerve terminals of the external layer of the median eminence. The effects were marked in hypophysectomized males and females, with or without castration, and less marked in castrated males and females and in normal males. In normally cycling females, prolactin caused a blockade of the cyclic changes in activity in the tubero-infundibular DA neurons, resulting in constant high turnover as is found in diestrus. Prolactin had no effects on the ascending noradrenaline (NA) neurons terminating in the hypothalamus or on the nigro-neostriatal DA neurons. During lactation, an endocrinological state with high prolactin secretion, the DA turnover in the external layer of the median eminence is very high. Both this increase in DA turnover and the increase found during pregnancy were reduced by hypophysectomy or by administration of ergocornine methanesulfonate (ECO-580) and 2-Br-α-ergokryptine methanesulfonate (CB-154), two drugs that probably decrease prolactin secretion from the anterior pituitary. The present results suggest that the tubero-infundibular DA neurons are part of a feedback system involved in the regulation of prolactin secretion from the anterior pituitary. The hypothesis is forwarded that one of the functions of the tubero-infundibular DA neurons is to stimulate the secretion of PIF at the level of the median eminence, and thus to exert an inhibitory effect on prolactin release. Previous studies have indicated a role of the tubero-infundibular DA neurons in the regulation of FSHRF-LHRF release. This complex role of the DA neurons is discussed.