Sills T L, Vaccarino F J
Section on Behavioral Neuropharmacology, NIMH, Bethesda, MD 20892-1380, USA.
Peptides. 1996;17(4):593-9. doi: 10.1016/0196-9781(96)00032-0.
Cholecystokinin (CCK) decreases food intake in a variety of species when administered systemically or centrally. Moreover, both CCKA and CCKB receptor mechanisms have been implicated in CCK's effects on feeding. Previous work done in our laboratory has shown that rats exhibit significant individual differences in the consumption of sugar. Moreover, intra-nucleus accumbens (Acc) administration of CCK reduced sugar consumption in rats with high baseline sugar intake (High) but did not affect sugar consumption in rats with low baseline sugar intake (Low). Thus, CCK mechanisms may contribute to individual differences in sugar intake observed in rats. The present study examined the involvement of endogenous CCK mechanisms in the regulation of sugar intake in Low and High rats. In Experiment 1, male Wistar rats were administered either the CCKA antagonist devazepide (0.001, 0.01, 0.1 mg/kg) or the CCKB antagonist L,365-260 (0.01, 0.1, 0.5 mg/kg) IP, and their intake of sugar and powdered lab chow recorded for 1 h. Experiment 2 was identical to Experiment 1 with the exception that rats received intra-Acc administrations of the selective CCKB antagonist PD-135158 (3, 10, 30 micrograms). Results showed that blockade of CCKB, but not CCKA receptors produced an increase in sugar consumption in Low rats and a decrease in sugar consumption in High rats. These effects were obtained with both systemic and intra-Acc administrations of a selective CCKB antagonist. These results suggest that endogenous CCK contributes to the mechanism regulating sugar consumption in Low and High rats through its actions on CCKB receptors in the Acc.
