Naltrexone, dopamine receptor agonists and antagonists, and food intake in rats: 2. 2-deoxy-D-glucose

Significantly greater inhibition of deprivation-induced food intake occurs following cotreatment with naltrexone and either the D1 antagonist, SCH-23390, the D2 agonist, quinpirole, or the D2 antagonist, haloperidol, relative to naltrexone alone. Cotreatment with the D1 agonist, SKF-38393, failed to...

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Published in:Pharmacology, biochemistry and behavior Vol. 49; no. 1; p. 205
Main Authors: Schaefer, L A, Koch, J E, Bodnar, R J
Format: Journal Article
Language:English
Published: United States 01-09-1994
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Summary:Significantly greater inhibition of deprivation-induced food intake occurs following cotreatment with naltrexone and either the D1 antagonist, SCH-23390, the D2 agonist, quinpirole, or the D2 antagonist, haloperidol, relative to naltrexone alone. Cotreatment with the D1 agonist, SKF-38393, failed to alter naltrexone's inhibition of deprivation-induced intake. The present study evaluated whether each of these D1 and D2 agonists and antagonists altered hyperphagia following 2-deoxy-D-glucose (2DG) themselves or in combination with naltrexone. Neither SKF-38393 (1-10 mg/kg) nor SCH-23390 (25-200 micrograms/kg) altered 2DG hyperphagia. Quinpirole (0.025-0.5 mg/kg) dose dependently decreased 2DG hyperphagia. 2DG hyperphagia was respectively increased and decreased by low (50 micrograms/kg) and high (500 micrograms/kg) doses of haloperidol. Cotreatment of SKF-38393 (0.1-1 mg/kg) and naltrexone potently enhanced the inhibition of 2DG hyperphagia relative to naltrexone alone. In contrast, cotreatment of naltrexone and either SCH-23390 (100-200 micrograms/kg) or quinpirole (0.025-0.05 mg/kg) inhibited 2DG hyperphagia in a manner similar to that of naltrexone alone. Finally, cotreatment of haloperidol (5-50 micrograms/kg) and naltrexone transiently enhanced the inhibition of 2DG hyperphagia relative to naltrexone alone.
ISSN:0091-3057
DOI:10.1016/0091-3057(94)90477-4