Cooper S J, Dourish C T, Barber D J
School of Psychology, University of Birmingham, U.K.
Pharmacol Biochem Behav. 1990 Jan;35(1):51-4. doi: 10.1016/0091-3057(90)90203-t.
The selective serotonin uptake inhibitor, fluoxetine (3.0-10 mg/kg), produced a significant dose-related suppression of palatable food consumption in nondeprived rats. The anorectic effect of fluoxetine (10 mg/kg) was not reversed by the potent and highly selective cholecystokinin receptor antagonist MK-329 [1-methyl-3-(2-indolyl) amino-5-phenyl-3H-1,4-benzodiazepin-2-one], administered in doses of 10-100 micrograms/kg. Fluoxetine (10 mg/kg) also significantly reduced the consumption of powdered laboratory chow in a 6-hr nocturnal free-feeding test. The anorectic effect in this paradigm was also not antagonized by MK-329. In contrast to previous data for d-fenfluramine (which enhances serotonin release), these results indicate that fluoxetine may suppress food intake by a mechanism which is independent of endogenous cholecystokinin.
选择性5-羟色胺再摄取抑制剂氟西汀（3.0 - 10毫克/千克）对未禁食大鼠的美味食物摄取产生了显著的剂量相关抑制作用。氟西汀（10毫克/千克）的厌食作用不会被剂量为10 - 100微克/千克的强效且高选择性胆囊收缩素受体拮抗剂MK - 329 [1 - 甲基 - 3 -（2 - 吲哚基）氨基 - 5 - 苯基 - 3H - 1,4 - 苯并二氮杂卓 - 2 - 酮]逆转。在6小时夜间自由进食试验中，氟西汀（10毫克/千克）也显著减少了实验室粉状饲料的摄入量。在此范例中的厌食作用同样未被MK - 329拮抗。与先前关于右芬氟拉明（可增强5-羟色胺释放）的数据相反，这些结果表明氟西汀可能通过一种独立于内源性胆囊收缩素的机制来抑制食物摄取。
