Lamberts S W, Verleun T, Oosterom R
Life Sci. 1985 Jun 10;36(23):2257-62. doi: 10.1016/0024-3205(85)90337-6.
The role of a direct effect of serotonin (5-HT) on PRL secretion at the pituitary level is uncertain. The present study investigated the mechanism of action of the serotonin receptor-blocking agent cyproheptadine on PRL release by normal cultured rat anterior pituitary cells. Cyproheptadine (10 nM-10 microM) and its metabolite desmethylcyproheptadine (a compound which has lost its affinity for serotonin receptors) directly inhibited PRL release, while serotonin, investigated over a wide concentration range, did not reverse this inhibition. The cyproheptadine-mediated inhibition of PRL-release could be completely prevented by 50 microM verapamil. Cyproheptadine strongly inhibited TRH-induced PRL release in the absence, but not in the presence of verapamil. Our studies suggest that cyproheptadine inhibits PRL release at the pituitary level by a blockade of calcium influx at the cell membrane, without affecting the movement of Ca2+ between intracellular compartments.
血清素（5-羟色胺，5-HT）在垂体水平对催乳素（PRL）分泌的直接作用尚不确定。本研究调查了血清素受体阻断剂赛庚啶对正常培养的大鼠垂体前叶细胞释放PRL的作用机制。赛庚啶（10 nM - 10 microM）及其代谢产物去甲基赛庚啶（一种对血清素受体失去亲和力的化合物）直接抑制PRL释放，而在较宽浓度范围内研究的血清素并不能逆转这种抑制作用。50 microM维拉帕米可完全阻止赛庚啶介导的PRL释放抑制。在不存在维拉帕米的情况下，赛庚啶强烈抑制促甲状腺激素释放激素（TRH）诱导的PRL释放，但在存在维拉帕米时则不然。我们的研究表明，赛庚啶通过阻断细胞膜上的钙内流在垂体水平抑制PRL释放，而不影响细胞内区室之间Ca2+的移动。
