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Recently, a number of studies have provided evidence suggesting that CCK and 5-HT interact in the control of food intake. However, the majority of these studies have relied on the administration of exogenous CCK to investigate potential interactions. The aim of the present study was to focus on the potential role of endogenous CCK in 5-HT-CCK interactions. Our prediction was that the CCKA antagonist, devazepide, alone would potentiate the hyperphagic effect of the 5-HT1A agonist, 8-OH-DPAT, in free-feeding rats. The results showed that devazepide, at a dose that had no intrinsic effect (1.0 mg/kg), did not enhance the hyperphagic effect of 8-OH-DPAT (100 and 300 micrograms/kg). This suggests that when serotonergic inhibitory activity is reduced by 5-HT1A-receptor stimulation, there is no compensatory increase of endogenous CCK activity to excite 5-HT neurons and thereby inhibit food intake.


Journal article


Physiol Behav

Publication Date





1337 - 1340


8-Hydroxy-2-(di-n-propylamino)tetralin, Animals, Benzodiazepinones, Devazepide, Drug Interactions, Eating, Hormone Antagonists, Hyperphagia, Male, Rats, Rats, Sprague-Dawley, Receptors, Cholecystokinin, Serotonin Receptor Agonists