The Influence of Pharmacological Manipulation of Serotonergic and Dopaminergic Mechanisms on Plasma Prolactin in Ovariectomized, Estrogen-Treated Rats*

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Abstract
Plasma prolactin was determined by radioimmunoassay in ovariectomized, estrogen-treated rats after the systemic administration of several serotonergic agonists and antagonists alone or in combination. Serotonin (5-HT), 5-hydroxytryptophan (5-HTP), and quipazine, a 5-HT agonist, each induced a marked yet transient release of prolactin. Fluoxetine, a 5-HT re-uptake blocker, combined with a small dose of 5-HTP but not 5-HT, also increased plasma levels of prolactin. Methysergide, cyproheptadine and SQ 10,631 [2-chloro-2''-[3-(dimethylamino)propyl]thio-cinnamanilide hydrochloride], suspected 5-HT receptor antagonists, induced small, yet significant, depressions of basal plasma prolactin levels. In addition, 1 of these antagonists, methysergide, significantly increased plasma prolactin. This increase could be blocked by apomorphine. Of the three 5-HT antagonists used, only methysergide blocked 5-HT and 5-HTP-induced elevations in plasma prolactin. The pretreatment of rats with apomorphine completely blocked prolactin release induced by 5-HTP and all doses of 5-HT except 20 mg/kg, whereas these serotonergic-induced elevations were not additive to the marked increase in prolactin induced by pimozide. 5-HT and 5-HTP apparently exert stimulatory effects on plasma prolactin probably by action at 5-HT receptors in the CNS. The effects of 5-HT and 5-HTP do not appear identical. There apparently is direct antagonism between a serotonergic system and the dopaminergic system that inhibits prolactin secretion.