Lack of evidence that the central serotoninergic system plays a role in the activation of prolactin secretion following inhibition of dopamine synthesis or blockade of dopamine receptors in the male rat.
Administration of alpha MT to inhibit catecholamine synthesis or dopamine (DA) receptor blockade with spiroperidol had no effect on the hypothalamic concentration of 5HT or 5HIAA. Fluoxetine to block serotonin uptake had no influence on the elevation of serum prolactin levels induced by alpha MT or DA receptor blockers and conversely alpha MT did not influence the prolactin-releasing action of 5HTP alone or in combination with fluoxetine. Depletion of brain serotonin stores with p-chlorophenylalanine did not affect the prolactin-releasing action of alpha MT or DA receptor blockers. In contrast, the serotonin blocker methysergide, but not cyproheptadine, inhibited the prolactin-releasing effect of alpha MT or alpha-flupentixol, a DA receptor blocker, but not of spiroperidol, another DA receptor blocker. The intensity of the inhibition induced by methysergide paralleled the intensity of inhibition induced by apomorphine. Methysergide conspicuously lowered serum prolactin in animals with electrolytic destruction of the median eminence, whereas cyproheptadine had only a slight effect. The prolactin-inhibiting effect of methysergide could be prevented by pretreatment of the lesioned rats with spiroperidol. It is concluded (1) that elimination of the influence of the DA system does not activate the central serotoninergic system; (2) that activity of the serotoninergic system has no role in the activation of prolactin secretion induced by suppression of the inhibitory dopaminergic influence, and (3) that the inhibiting action of methysergide on the prolactin-releasing effect of alpha MT or alpha-flupentixol is due to its dopamine receptor agonist activity rather than to blockade of serotonin receptors.
D006916:5-Hydroxytryptophan / Q000494:pharmacology; D000818:Animals; D001058:Apomorphine / Q000494:pharmacology; D003533:Cyproheptadine / Q000494:pharmacology; D003864:Depression, Chemical; D004298:Dopamine / Q000096:biosynthesis*; D018492:Dopamine Antagonists; D010134:Fenclonine / Q000494:pharmacology; D005473:Fluoxetine / Q000494:pharmacology; D005475:Flupenthixol / Q000494:pharmacology; D007031:Hypothalamus / Q000502:physiology*; D008297:Male; D008784:Methysergide / Q000494:pharmacology; D011388:Prolactin / Q000378:metabolism*; D051381:Rats; D011954:Receptors, Dopamine / Q000502:physiology*; D011985:Receptors, Serotonin / Q000502:physiology*; D013134:Spiperone / Q000494:pharmacology; D013268:Stimulation, Chemical; D014443:Tyrosine / Q000031:analogs & derivatives / Q000494:pharmacology
D018492:Dopamine Antagonists; D011954:Receptors, Dopamine; D011985:Receptors, Serotonin; D005473:Fluoxetine; D003533:Cyproheptadine; D014443:Tyrosine; D013134:Spiperone; D011388:Prolactin; D006916:5-Hydroxytryptophan; D005475:Flupenthixol; D001058:Apomorphine; D010134:Fenclonine; D004298:Dopamine; D008784:Methysergide