SYSTEMIC ADMINISTRATION OF CHOLECYSTOKININ (CCK) INHIBITS OPERANT WATER-INTAKE IN RATS - IMPLICATIONS FOR THE CCK-SATIETY HYPOTHESIS

Authors
Citation
Is. Ebenezer, SYSTEMIC ADMINISTRATION OF CHOLECYSTOKININ (CCK) INHIBITS OPERANT WATER-INTAKE IN RATS - IMPLICATIONS FOR THE CCK-SATIETY HYPOTHESIS, Proceedings - Royal Society. Biological Sciences, 263(1369), 1996, pp. 491-496
Citations number
32
Categorie Soggetti
Biology
ISSN journal
09628452
Volume
263
Issue
1369
Year of publication
1996
Pages
491 - 496
Database
ISI
SICI code
0962-8452(1996)263:1369<491:SAOC(I>2.0.ZU;2-0
Abstract
The demonstration that intraperitoneal administration of the sulphated octapeptide of cholecystokinin (CCK-8S) inhibits food but not water i ntake in rats, has led to the hypothesis that endogenous peripheral CC K acts as a food-specific satiety factor. As water-deprived rats given free access to water can satisfy their thirst fairly rapidly, it is c onceivable that the apparent lack of effect of CCK on water intake rep orted previously may have been because the animals had satisfied their thirst before the full effects of the peptide had become apparent. To test this possibility, the effects of intraperitoneal (i.p.) administ ration of CCK-8S, at doses that had previously been shown to inhibit f ood intake, were investigated on water intake in rats trained to make operant responses for water reinforcements. Such a paradigm has the me rit of slowing down the rate at which a water-deprived rat can quench its thirst, thus extending the period over which the effects of CCK-8S on water intake may be assessed. CCK-8S (2, 4 or 8 mu g kg(-1), i.p.) produced a dose-related suppression of operant water intake in 16 h w ater-deprived rats during the first 30 min after administration. Addit ional experiments indicated that, as with feeding, CCK-8S inhibits wat er intake by an action at peripheral CCKA receptors. These findings ha ve important implications for the CCK-satiety hypothesis as they show that the effect of the peptide on ingestive behaviours in the rat is n ot specific for food intake and suggest that it is unlikely that CCK i s a mediator of satiety.