ROLE OF THE CENTRAL SEROTONINERGIC SYSTEM IN THE REGULATION OF THE SECRETION OF THYROTROPIN AND PROLACTIN - THYROTROPIN-INHIBITING AND PROLACTIN-RELEASING EFFECTS OF 5-HYDROXYTRYPTAMINE AND QUIPAZINE IN THE MALE-RAT

Injection of 5-hydroxytryptamine (5-HT) into the third ventricle of unanesthetized, unrestrained rats induced a dose-related decrease of serum TSH and an increase of serum PRL. Quipazine, a 5-HT receptor stimulant, elicited similar hormonal changes when administered intraventricularly or systemically. The effects of quipazine were augmented in animals depleted of central 5-HT stores, presumably as a consequence of supersensitivity of central serotonin receptors, but they were abolished in rats with electrolytic lesions of the median eminence. Quipazine did not influence the stimulation of TSH secretion evoked by exogenous TRH. Methysergide, a 5-HT receptor blocker, had different effects on responses elicited by 5- HT or quipazine; while preventing TSH and PRL changes induced by intraventricular 5-HT and the rise of serum PRL by quipazine, it did not antagonize the effects of quipazine on TSH secretion. On the other hand, cyproheptadine, also a 5-HT receptor blocker, abolished the inhibitory effects of quip azine on TSH secretion but was only partially effective in antagonizing its PRL-releasing action. On the basis of these results, it is concluded that activation of central serotonin receptors by 5-HT or quipazine inhibits the release of hypothalamic TRH, which in turn leads to a decrease of serum TSH. The stimulation of PRL secretion by 5-HT and quipazine adds further support to the concept of serotoninergic regulation of the secretion of this hormone. The differential effects of the 5-HT receptor blockers on TSH and PRL responses are difficult to interpret; existence of functionally different pools of serotoninergic neurons with differential affinities of their postsynaptic receptors to methysergide and cyprohepatidine might be envisioned as a hypothetical possibility. It is also necessary to consider the possibility that activation of the dopamine receptors of the pituitary lactotroph by methysergide may have played a role in the inhibiting effect on PRL secretion. © 1979 by The Endocrine Society.