Histaminergic Regulation of Prolactin Secretion: Involvement of Serotoninergic Neurons

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Abstract
The possible involvement of the serotoninergic system in histamine-induced PRL secretion was studied in urethane anesthetized male rats. Intracerebroventricular infusion of histamine (30 .mu.g) stimulated PRL secretion 10-fold. This effect was mimicked by the H2-receptor agonist dimaprit (300 .mu.g), while the H1-receptor agonist 2-thiazolylethylamine (140 .mu.g) had no effect. Pretreatment with the serotonin receptor blockers methysergide (2.5 mg/kg i.p.) or ketanserin (2.5 or 10.0 mg/kg i.p.) reduced the PRL peak response to histamine 75,54, or 58%, respectively. During serotonin receptor blockage, dimaprit had a stimulatory effect similar to that of histamine, while 2-thiazolylethylamine had no effect. Intraarterial infusion of histamine (420 .mu.g) stimulated PRL secretion 6-fold. This effect was mimicked by the H1-receptor agonist 2-thiazolylethylamine (1,900 .mu.g), while the H2-receptor agonist dimaprit (3,000 .mu.g) had no effect. Pretreatment with methysergide (2.5 mg/kg i.p.) or ketanserin (2.5 or 10.0 mg/kg i.p) reduced the peak response to histamine 54, 54 or 51%, respectively. The effect of histamine was mimicked by 2-thiazolylethlamine, while dimaprit slightly inhibited the PRL secretion. The antiserotoninergic activity of methysergide and ketanserin was demonstrated by their ability to prevent the PRL-releasing effect to serotonin. The effects of methysergide and ketanserin were not due to dopamine-like activity, since none of the drugs affected basal PRL secretion and since the dopamine receptor antagonist pimozide did not prevent the inhibitory effect of methysergide on the histamine-induced PRL release. The findings indicate that histamine-stimulated PRL secretion is mediated in part by serotoninergic neurons.