Inhibition of deprivation-induced feeding by naloxone and cholecystokinin in rats: Effects of central alloxan

Abstract

Central administration of alloxan reduces the hyperphagic, but not the hyperglycemic response to glucoprivation by presumably acting upon brain glucoreceptors or a glucoprivic control mechanism. The present study evaluated whether central alloxan pretreatment respectively altered the dose-dependent suppressant effects upon deprivation (24-hr)-induced feeding of naloxone (0.01–10 mg/kg, IP) and cholecystokinin octapeptide (CCK-8: 1–8 μg/kg, IP) in rats. Central alloxan (200 μg, ICV) failed to alter body weight, free-feeding and deprivation-induced feeding. Both naloxone and CCK-8 produced significant dose-dependent inhibitions of deprivation-induced feeding in control rats. Central alloxan treatment significantly diminished peak naloxone hypophagia induced by 2.5 and 10 mg/kg doses, and CCK-8 hypophagia induced by the 1 and 4 μg/kg doses. Coadministration of 3 M D-glucose, which acts as a cytoprotectant against alloxan-induced diabetes, blocked the attenuating actions of alloxan upon naloxone and CCK-8 hypophagia. These data indicate the effectiveness of central alloxan in restricting the ability of pharmacological agents to either stimulate or inhibit food intake in rats without altering basal intake or body weight maintenance.