beta-funaltrexamine and maltodextrin

Different central opioid receptor subtypes participate in the mediation of intakes of simple (sucrose: mu, kappa 1) and complex (maltose dextrin: mu) carbohydrates as well as deprivation-induced water intake (mu) under real-feeding and real-drinking conditions. An identical pattern of mu and kappa 1 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 micrograms), mu (beta-funaltrexamine: 1-20 micrograms), mu 1 (naloxonazine: 50 micrograms), kappa 1 (nor-binaltorphamine: 1-20 micrograms), delta 1 ([D-Ala2, Leu5, Cys6]-enkephalin: 10-40 micrograms) or delta 2 (naltrindole isothiocyanate: 20 micrograms) 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 kappa 1 (69%) or delta 1 (59%) opioid antagonism, was significantly increased by mu 1 antagonism (43%), and was not significantly affected by either mu or delta 2 opioid antagonism. Deprivation-induced water intake in sham drinking rats was significantly reduced by either mu (41%), mu 1 (28%), delta 1 (48%) or delta 2 (28%) opioid antagonism, but was not significantly affected by kappa 1 opioid antagonism. The difference in opioid receptor subtype mediation of maltose dextrin intake in real feeding and sham feeding conditions suggest that kappa 1 and delta 1 receptors are involved in the orosensory mechanisms supporting maltose dextrin intake, while mu 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 drink

Topics: Animals; Dose-Response Relationship, Drug; Drinking; Eating; Enkephalin, Leucine-2-Alanine; Injections, Intraventricular; Male; Naloxone; Naltrexone; Narcotic Antagonists; Polysaccharides; Rats; Rats, Sprague-Dawley; Receptors, Opioid, delta; Receptors, Opioid, kappa; Receptors, Opioid, mu; Water Deprivation

Opioid modulation of ingestion includes general opioid antagonism of deprivation-induced water intake and intake of sucrose and saccharin solutions. Previous studies using selective subtype antagonists indicated that opioid effects upon deprivation-induced water intake occurred through the mu2 receptor and that opioid effects upon sucrose intake occurred through kappa and mu2 receptors. The present study compared the effects of intracerebroventricular administration of opioid receptor subtype antagonists upon intakes of a saccharin solution and a maltose dextrin (MD) solution to determine which receptor subtypes were involved in modulation of ingestion of different preferred tastants. Significant reductions in saccharin intake (1 h) occurred following naltrexone (20-50 micrograms: 66%) and naltrindole (delta, 20 micrograms: 75%), whereas [D-Ala2, Leu5, Cys6]-enkephalin (DALCE, delta 1, 40 micrograms: 45%) had transient (5 min) effects. Neither beta-funaltrexamine (B-FNA, mu), naloxonazine (mu1), nor nor-binaltorphamine (Nor-BNI, kappa) significantly altered saccharin intake. Significant reductions in MD intake (1 h) occurred following naltrexone (5-50 micrograms: 69%) and B-FNA (1-20 micrograms: 38%). MD intake was not reduced by naltrindole, DALCE, naloxonazine and Nor-BNI. Peak antagonist effects were delayed (20-25 min) to reflect interference with the maintenance, rather than the initiation of saccharin or MD intake. Comparisons of opioid antagonist effects across intake situations revealed that naltrexone had consistently low ID40 values for saccharin (29 nmol), MD (25 nmol), sucrose (6 nmol) and deprivation (38 nmol) intake. Despite its significant effects relative to naloxonazine, B-FNA had significantly higher ID40 values for saccharin (800 nmol), MD (763 nmol) and sucrose (508 nmol) relative to deprivation (99 nmol) intake, suggesting that mu2 receptors may be mediating maintenance of intake rather than taste effects. Nor-BNI had low ID40 values for intake of sucrose (4 nmol), but not for saccharin (168 nmol), MD (153 nmol) and deprivation (176 nmol), suggesting that kappa receptors may mediate ingestion of sweet-tasting stimuli. That delta (naltrindole: ID40 = 60 nmol), but not delta 1 (DALCE: ID40 = 288 nmol) antagonists consistently reduce saccharin intake suggests a role for the delta 2 receptor subtype in the modulation of hedonic orosensory signals.

Topics: Animals; Drinking Behavior; Enkephalin, Leucine-2-Alanine; Injections, Intraventricular; Male; Naloxone; Naltrexone; Narcotic Antagonists; Polysaccharides; Rats; Rats, Sprague-Dawley; Saccharin