Van de Kar L D, Bethea C L
Neuroendocrinology. 1982 Oct;35(4):225-30. doi: 10.1159/000123386.
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 pretreatment 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.
给大鼠注射释放血清素的药物DL-对氯苯丙胺（PCA）会导致血浆催乳素水平呈剂量依赖性升高。给药后2小时效果达到最大。血清素合成抑制剂对氯苯丙氨酸甲酯（PCPA）预先给药可阻止PCA的作用。PCPA预处理不能阻止血清素激动剂喹哌嗪给药后血浆催乳素水平的升高，这与喹哌嗪的突触后受体相互作用一致。为了确定涉及哪些血清素能神经元，在背侧或中缝核受损的大鼠中测定了对PCA的催乳素反应。在PCA激发前2周，通过局部注射5,7-二羟基色胺（5,7-DHT）在经去甲丙咪嗪预处理的大鼠中造成损伤。在背侧中缝核受损的大鼠中，PCA对催乳素分泌的作用显著减弱。相比之下，中缝核损伤并不能阻止PCA对血浆催乳素水平的作用。总之，这些数据支持血清素释放增加催乳素分泌的假说。此外，这些数据表明背侧中缝核中的血清素能神经元是可介导催乳素分泌增加的神经通路的一部分。
