Different central opioid receptor subtype antagonists modify maltose dextrin and deprivation-induced water intake in sham feeding and sham drinking rats

Different central opioid receptor subtypes participate in the mediation of intakes of simple (sucrose: μ, κ₁ and complex (maltose dextrin: μ) carbohydrates as well as deprivation-induced water intake (μ) under real-feeding and real-drinking conditions. An identical pattern of μ and κ₁ mediation of sucrose intake was observed in sham-feeding rats as well, suggesting their actions on orosensory mechanisms supporting sucose intake. The present study examined whether centrally administered general (naltrexone: 1–50 μg), μ (β-funaltrexamine: 1–20 μg), μ₁ (naloxonazine: 50 μg), κ₁ (nor-binaltorphamine: 1–20 μg), δ₁ ([d-Ala², Leu⁵, Cys⁶]-enkephalin: 10–40 μg) or δ₂2 (naltrindole isothiocyanate: 20 μg) opioid subtype antagonists altered either maltose dextrin (10%) intake during sham feeding or deprivation (24 h)-induced water intake during sham drinking in rats with gastric fistulas. Sham feeding significantly increased maltose dextrin intake (180%) and sham drinking significantly increased deprivation-induced water intake (256%) over a 60 min time course. Naltrexone significantly and dose-dependently reduced maltose dextrin intake (78%) in sham feeding rats, and deprivation-induced water intake (51%) in sham drinking rats. Maltose dextrin intake in sham feeding rats was significantly reduced by either κ₁ (69%) or δ₁ (59%) opioid antagonism, was significantly increased by μ₁ antagonism (43%), and was not significantly affected by either μ or δ₂ opioid antagonism. Deprivation-induced water intake in sham drinking rats was significantly reduced by either μ (41%), μ₁ (28%), δ₁ (48%) or δ₈ (28%) opioid antagonism, but was not significantly affected by κ₁ opioid antagonism. The difference in opioid receptor subtype mediation of maltose dextrin intake in real feeding and sham feeding conditions suggest that κ₁ and δ₁ receptors are involved in the orosensory mechanisms supporting maltose dextrin intake, while μ receptors are involved in the ingestive and post-ingestive mechanisms supporting maltose dextrin intake. The different patterns of opioid involvement in sucrose and maltose dextrin intake in sham feeding and real feeding conditions provide further support for the hypothesis that at least two different carbohydrate taste systems exist. The difference in opioid receptor subtype mediation of deprivation-induced water intake in real drinking and sham drinking conditions may reflect the removal in the sham drinking condition of a μ-mediated prerestorative satiety mechanism, and the unmasking of other opioid-mediated signalling mechanisms.