title: Dietary modulation of mu and kappa opioid receptor-mediated analgesia.
abstract: Research has demonstrated that intake of palatable carbohydrates and fats enhanced morphine-induced analgesia (MIA) in Sprague-Dawley rats. To determine if the effects of palatable foods on nociceptive responses would generalize to other strains of animals and other opioid agonists, the present experiments investigated whether intake of palatable foods would: a) alter MIA in Long-Evans rats, and b) alter analgesia produced by drugs acting at kappa opioid receptors. In experiment 1, adult male Long-Evans rats were fed Purina chow alone or chow and either a 32% sucrose solution, a 0.15% saccharin solution, or hydrogenated vegetable fat. Using a tail-flick apparatus, nociceptive responses, measured as percent maximal possible effect (%MPE), were examined after morphine administration [0.0, 1.0, 3.0, and 6.0 mg/kg subcutaneously (SC)]. %MPEs varied directly as a function of dose and were significantly greater for rats fed chow and either sucrose or fat than for rats fed chow alone or chow and saccharin. Experiment 2 compared the analgesic effect of the kappa opioid receptor agonist U50,488H (0, 5.0, 10.0, and 20.0 mg/kg SC) in rats fed chow alone or chow and a 32% sucrose solution. Administration of U50,488H led to analgesia. However, %MPEs did not vary directly as a function of dose. %MPEs of rats fed chow and sucrose were significantly greater than those of rats fed chow alone after injections of 10.0 and 20.0 mg/kg U50,488H. Experiment 3 compared the analgesic effect of U50,488H (5.0, 10.0, 15.0, and 20.0 mg/kg SC) in rats fed chow alone or chow and either a 0.15% saccharin solution or hydrogenated vegetable fat. Administration of U50,488H led to analgesia. However, %MPEs did not vary directly as a function of dose or as a function of diet. %MPEs of rats fed chow and fat were significantly greater than those of rats fed chow alone after injection of 5.0 mg/kg U50,488H.
authors.affiliation: Department of Psychology, Tufts University, Medford, MA 02155, USA.
authors.forename: R B
authors.initials: RB
authors.lastname: Kanarek
authors.forename: J
authors.initials: J
authors.lastname: Przypek
authors.forename: K E
authors.initials: KE
authors.lastname: D'Anci
authors.forename: R
authors.initials: R
authors.lastname: Marks-Kaufman
mesh_terms: D019900:3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer; D000700:Analgesics / Q000494:pharmacology; D000701:Analgesics, Opioid / Q000494:pharmacology*; D000818:Animals; D004032:Diet; D004041:Dietary Fats / Q000494:pharmacology; D004435:Eating / Q000502:physiology; D004734:Energy Metabolism / Q000187:drug effects / Q000502:physiology; D008297:Male; D009020:Morphine / Q000494:pharmacology; D010147:Pain Measurement / Q000187:drug effects*; D017288:Pain Threshold / Q000187:drug effects; D011759:Pyrrolidines / Q000494:pharmacology; D051381:Rats; D017473:Receptors, Opioid, kappa / Q000819:agonists*; D017450:Receptors, Opioid, mu / Q000819:agonists*; D013395:Sucrose / Q000494:pharmacology; D015430:Weight Gain / Q000502:physiology
chemical_list: D000700:Analgesics; D000701:Analgesics, Opioid; D004041:Dietary Fats; D011759:Pyrrolidines; D017473:Receptors, Opioid, kappa; D017450:Receptors, Opioid, mu; D013395:Sucrose; D019900:3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer; D009020:Morphine