Quattrone A, Schettini G, Di Renzo G F, Preziosi P
Arch Int Pharmacodyn Ther. 1979 Mar;238(1):42-9.
The purpose of the present study was to investigate the possible interaction between serotonergic and dopaminergic neurons in regulating prolactin (PRL) secretion. We have examined the effect of quipazine, a drug which has been reported to increase plasma PRL levels by acting through a serotonergic mechanism, on PRL release in rats pretreated with penfluridol or alpha-methyl-p-tyrosine (alpha-MPT). The effect of d-fenfluramine, a serotonin releaser, on plasma PRL levels in animals pretreated with penfluridol was also studied. Penfluridol or alpha-MPT treatments significantly stimulated PRL secretion. Quipazine also increased plasma PRL levels in normal male rats. However, this drug was not able to further stimulate PRL release in animals pretreated with penfluridol or alpha-MPT. Like quipazine, d-fenfluramine increased plasma PRL levels in normal rats but it failed to further stimulate PRL secretion in penfluridol-pretreated animals. These findings support the hypothesis that serotonin may stimulate PRL release through an inhibition of dopaminergic neurons.
本研究的目的是探讨5-羟色胺能神经元和多巴胺能神经元在调节催乳素（PRL）分泌过程中可能存在的相互作用。我们研究了喹哌嗪（一种据报道通过5-羟色胺能机制作用来提高血浆PRL水平的药物）对用五氟利多或α-甲基对酪氨酸（α-MPT）预处理的大鼠PRL释放的影响。还研究了5-羟色胺释放剂d-芬氟拉明对用五氟利多预处理的动物血浆PRL水平的影响。五氟利多或α-MPT处理显著刺激了PRL分泌。喹哌嗪也提高了正常雄性大鼠的血浆PRL水平。然而，该药物在五氟利多或α-MPT预处理的动物中无法进一步刺激PRL释放。与喹哌嗪一样，d-芬氟拉明提高了正常大鼠的血浆PRL水平，但在五氟利多预处理的动物中未能进一步刺激PRL分泌。这些发现支持了5-羟色胺可能通过抑制多巴胺能神经元来刺激PRL释放的假说。
