Meltzer H Y, Simonovic M, Gudelsky G A
Eur J Pharmacol. 1985 Mar 26;110(1):143-6. doi: 10.1016/0014-2999(85)90042-1.
Intraperitoneal administration of phencyclidine (PCP, 2.5-20 mg/kg) produced a dose-related inhibition of the increase in serum PRL concentrations produced by alpha-methylparatyrosine (AMPT) or reserpine, but not morphine. Phencyclidine was more potent in antagonizing the PRL-releasing effect of reserpine than that of AMPT, suggesting a greater effect of PCP on the cytoplasmic than the storage dopamine (DA) pool. Phencyclidine had no effect on PRL release from rat pituitary glands in vitro. Intravenous administration of PCP (10 mg/kg) to anesthetized male rats produced a two-fold increase in pituitary stalk (DA) concentrations, suggesting that PCP inhibits rat serum PRL by increasing the release of DA from the tuberoinfundibular neurons, and possibly by blocking its reuptake as well.
腹腔注射苯环己哌啶(PCP,2.5 - 20毫克/千克)可剂量依赖性地抑制由α-甲基对酪氨酸(AMPT)或利血平引起的血清催乳素(PRL)浓度升高,但对吗啡引起的升高无抑制作用。与AMPT相比,苯环己哌啶拮抗利血平的PRL释放作用更强,这表明PCP对细胞质多巴胺(DA)池的作用大于对储存DA池的作用。苯环己哌啶对体外培养的大鼠垂体释放PRL没有影响。对麻醉的雄性大鼠静脉注射PCP(10毫克/千克)可使垂体柄(DA)浓度增加两倍,这表明PCP通过增加结节漏斗神经元释放DA,并可能还通过阻断其再摄取来抑制大鼠血清PRL。