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

Abstract

Significantly greater inhibition of deprivation-induced food intake occurs following cotreatment with naltrexone and either the D 1 antagonist, SCH-23390, the D 2 aqonist, quinpirole, or the D 2 antagonist, haloperidol, relative to naltrexone alone. Cotreatment with the D 1, agonist, SKF-38393, failed to alter naltrexone's inhibition of deprivation-induced intake. The present study evaluated whether each of these D 1 and D 2 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 μg/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 μg/kg) and high (500 μg/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 μg/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 μg/kg) and naltrexone transiently enhanced the inhibition of 2DG hyperphagia relative to naltrexone alone.