Toth P, Shaw C, Perlanski E, Grupp L A
Department of Pharmacology, University of Toronto, Ontario, Canada.
Pharmacol Biochem Behav. 1990 Feb;35(2):493-5. doi: 10.1016/0091-3057(90)90193-l.
The putative satiety peptide cholecystokinin octapeptide (CCK-8) has been shown to reduce ethanol intake induced by prior fluid deprivation. Since fluid-deprived animals tend to reduce their food intake and consequently become hungry, the ability of CCK-8 to reduce ethanol intake might be limited to conditions where the motivation for food and fluid are accentuated. The present study assessed this possibility by examining the effect of peripheral injections of CCK-8 on voluntary ethanol intake fostered by the limited access procedure which uses food- and water-sated rats. Under these conditions CCK-8 still produced a dose-dependent decrease in ethanol intake. These results demonstrate that CCK-8 reduces ethanol intake even in the absence of hunger and thirst drives.
公认的饱腹感肽八肽胆囊收缩素（CCK - 8）已被证明可减少先前液体剥夺诱导的乙醇摄入量。由于液体剥夺的动物往往会减少食物摄入量并因此变得饥饿，CCK - 8减少乙醇摄入量的能力可能仅限于食物和液体动机增强的情况。本研究通过检查外周注射CCK - 8对采用食物和水饱足大鼠的限时获取程序所促进的自愿乙醇摄入量的影响，评估了这种可能性。在这些条件下，CCK - 8仍使乙醇摄入量呈剂量依赖性减少。这些结果表明，即使在没有饥饿和口渴驱动力的情况下，CCK - 8也能减少乙醇摄入量。
