Eberle-Wang K, Simansky K J
Department of Pharmacology, Medical College of Pennsylvania, Philadelphia 19129.
Pharmacol Biochem Behav. 1992 Nov;43(3):943-7. doi: 10.1016/0091-3057(92)90429-j.
A role has been proposed for cholecystokinin (CCK)-A-type receptors in mediating the anorectic action produced by serotonergic stimulation in rats. We examined the effect of pretreatment with the CCK-A antagonist devazepide (DVZ) on anorexia produced by peripheral administration of serotonin [5-hydroxytryptamine (5-HT)] or CCK-8 in 3-h food-deprived rats consuming a 30-min test meal of sweetened mash. The anorectic effect of CCK-8 (4.0 nmol/kg, IP) was antagonized in a dose-dependent manner by DVZ (0.03, 0.10, and 0.30 mumol/kg, IP), with even the lowest dose producing a significant reversal. Under identical testing conditions, a supramaximal dose of DVZ (.75 mumol/kg) did not attenuate the reductions in food intake produced by either a moderate (4.0 mumol/kg) or a high dose (10.0 mumol/kg) of 5-HT. These data confirm established findings that the anorectic action of peripheral CCK depends upon CCK-A receptors. However, peripherally administered 5-HT reduces food intake independently of CCKergic function.
胆囊收缩素（CCK）-A型受体在介导大鼠5-羟色胺能刺激产生的厌食作用中所起的作用已被提出。我们研究了用CCK-A拮抗剂地伐西匹（DVZ）预处理对3小时未进食、食用30分钟甜味糊测试餐的大鼠外周给予5-羟色胺（5-HT）或CCK-8所产生的厌食作用的影响。CCK-8（4.0 nmol/kg，腹腔注射）的厌食作用被DVZ（0.03、0.10和0.30 μmol/kg，腹腔注射）以剂量依赖的方式拮抗，即使是最低剂量也能产生显著的逆转。在相同的测试条件下，超最大剂量的DVZ（0.75 μmol/kg）并未减弱中等剂量（4.0 μmol/kg）或高剂量（10.0 μmol/kg）的5-HT所引起的食物摄入量减少。这些数据证实了已有的研究结果，即外周CCK的厌食作用取决于CCK-A受体。然而，外周给予的5-HT独立于CCK能功能而减少食物摄入量。
