INDIVIDUAL-DIFFERENCES IN THE FEEDING RESPONSE TO CCKB ANTAGONISTS - ROLE OF THE NUCLEUS-ACCUMBENS

Citation
Tl. Sills et Fj. Vaccarino, INDIVIDUAL-DIFFERENCES IN THE FEEDING RESPONSE TO CCKB ANTAGONISTS - ROLE OF THE NUCLEUS-ACCUMBENS, Peptides, 17(4), 1996, pp. 593-599
Citations number
48
Categorie Soggetti
Biology
Journal title
ISSN journal
01969781
Volume
17
Issue
4
Year of publication
1996
Pages
593 - 599
Database
ISI
SICI code
0196-9781(1996)17:4<593:IITFRT>2.0.ZU;2-J
Abstract
Cholecystokinin (CCK) decreases food intake in a variety of species wh en administered systemically or centrally. Moreover, both CCKA and CCK B receptor mechanisms have been implicated in CCK's effects on feeding . Previous work done in our laboratory has shown that rats exhibit sig nificant individual differences in the consumption of sugar. Moreover, intra-nucleus accumbens (Acc) administration of CCK reduced sugar con sumption in rats with high baseline sugar intake (High) but did not af fect sugar consumption in rats with low baseline sugar intake (Low). T hus, 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 an d High rats. In Experiment 1, male Wistar rats were administered eithe r the CCKA antagonist devazepide (0.001, 0.01, 0.1 mg/kg) or the CCK, antagonist L,365-260 (0.01, 0.1, 0.5 mg/kg) IP, and their intake of su gar and powdered lab chow recorded for 1 h. Experiment 2 was identical to Experiment 1 with the exception that rats received intra-Acc admin istrations of the selective CCKB antagonist PD-135158 (3, 10, 30 mu g) . Results showed that blockade of CCKB, but not CCKA, receptors produc ed an increase in sugar consumption in Low rats and a decrease in suga r consumption in High rats. These effects were obtained with both syst emic and intra-Acc administrations of a selective CCKB antagonist. The se results suggest that endogenous CCK contributes to the mechanism re gulating sugar consumption in Low and High rats through its actions on CCKB receptors in the Acc.