Cholecystokinin-induced satiation with ethanol: effects of lighting cycle and limited access procedures

Abstract

Cholecystokinin (CCK) is a brain-gut neuropeptide and hormone previously shown to inhibit alcohol intake in water- or food-deprived rats. The effects of CCK and the phase of lighting cycle on alcohol intake in rats were investigated in a comparison of limited access and water-restriction procedures. The limited access procedure (LAP) is a recently developed technique for inducing free-choice alcohol consumption in nondeprived animals. Two groups of 12 male rats each were maintained in either normal or reversed 12:12 L:D lighting cycles and simultaneously given 40 minutes' access to 6% w/v ethanol and water in nonhome cages. After adaptation to this procedure, CCK octapeptide (0.5-16 micrograms/kg) was injected IP prior to access to fluids. During LAP, CCK reduced alcohol intake and increased water intake more potently in the dark phase. These effects of CCK were more reliable when the design was replicated, which suggests the importance of acquired expectancies for the development of CCK's actions. CCK more effectively reduced alcohol intake in LAP, than in a 23.3-h water-deprivation procedure for inducing alcohol intake in a 2-bottle choice test with water. However, CCK was less so effective in LAP, than in the water-deprivation procedure when alcohol was presented alone in a 1-bottle test. The alcohol satiation effect of CCK is independent of prior deprivation and not an artifact of thirst reduction, debilitation, or conditioned aversion, because CCK strongly increased water intake in the limited access procedure, and ethanol preference remained robust after experience with CCK. CCK may operate endogenously as a specific factor in satiation with ethanol.