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The introduction of potent cholecystokinin (CCK) receptor antagonists, selective for either the CCK-A or the CCK-B subtype, has provided a great impetus to the study of activity of endogenous CCK in relation to the control of feeding. This paper reviews experiments in which devazepide (a selective CCK-A receptor antagonist) and L-365,260 (a selective CCK-B-gastrin receptor antagonist) have been used. Both compounds increase food consumption (under certain conditions) and postpone the onset of satiety. L-365,260 is the more potent, suggesting a role for central CCK-B type receptors in satiety. In addition, use of CCK antagonists permits the study of important functional interactions between CCK and other neurochemical factors that serve to control feeding. Thus, devazepide, but not L-365,260, blocked the anorectic effect of either d-fenfluramine or serotonin. Hence, CCK-A type receptors appear to be involved in the anorectic effect of these drugs. This result serves as an example to illustrate a principle of cooperativity in the satiety-inducing effects of diverse neurochemical signals.

Original publication




Conference paper

Publication Date





291S - 295S


Animals, Benzodiazepinones, Biogenic Monoamines, Cholecystokinin, Devazepide, Drug Interactions, Phenylurea Compounds, Receptors, Cholecystokinin, Satiation, Serotonin