Pharmacological evidence that serotonergic stimulation of prolactin secretion is mediated via the dorsal raphe nucleus

Louis D. van de Kar, Cynthia L. Bethea

    Research output: Contribution to journalArticlepeer-review

    103 Scopus citations

    Abstract

    Administration of the serotonin-releasing drug DL-p-chloroamphetamine (PCA) to rats caused a dose-dependent increase in plasma prolactin levels. The effect was maximal 2 h after administration. The effect of PCA was prevented by prior administration of the serotonin synthesis inhibitor p-chlorophenylalanine-methyl ester (PCPA). PCPA pre-treatment did not prevent the increase in plasma prolactin levels after administration of the serotonin agonist quipazine which is consistent with a postsynaptic receptor interaction of quipazine. To determine which serotonergic neurons are involved, the prolactin responses to PCA were determined in rats sustaining lesions of the dorsal or median raphe nuclei. The lesions were produced in desmethylimipramine-pretreated rats by local injections of 5,7-dihydroxytryptamine (5,7-DHT) 2 weeks prior to the PCA challenge. In rats with dorsal raphe lesions, the effect of PCA on prolactin secretion was significantly attenuated. In contrast, median raphe lesions did not prevent the effect of PCA on plasma prolactin levels. In summary, these data support the hypothesis that release of serotonin increases prolactin secretion. In addition, these data suggest that serotonergic neurons in the dorsal raphe nucleus are part of a neural pathway which can mediate increases in prolactin secretion.

    Original languageEnglish (US)
    Pages (from-to)225-230
    Number of pages6
    JournalNeuroendocrinology
    Volume35
    Issue number4
    DOIs
    StatePublished - Jan 1 1982

    Keywords

    • 5,7-dihydroxytryptamine
    • Dorsal raphe nucleus
    • Parachloroamphetamine
    • Prolactin
    • Serotonin

    ASJC Scopus subject areas

    • Endocrinology, Diabetes and Metabolism
    • Endocrinology
    • Endocrine and Autonomic Systems
    • Cellular and Molecular Neuroscience

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