Opioid-receptor subtype agonist-induced enhancements of sucrose intake are dependent upon sucrose concentration

Selective mu ([D-Ala(2), N-Me-Phe(4), Gly-ol(5)]-enkephalin (DAMGO)), delta, ([D-Pen(2), D-Pen(5)]-enkephalin (DPDPE)), delta(2) ([D-Ala(2), Glu(4)]-Deltorphin (Delt II)), kappa, (U50488H) and kappa, (naloxone benzoylhydrazone (NalBzOH) opioid agonists each stimulate food intake in rats. Whereas studies with selective opioid antagonists implicate mu and kappa(1) receptors in the mediation of sucrose intake, studies with selective opioid agonists implicate mu and delta receptors in the mediation of saccharin intake. The present study determined if specific delta(1), delta(2), kappa(1), kappa(3) and mu opioid-receptor subtype agonists produced similar alter-ations in sucrose intake as a function of sucrose concentration (0.5%, 2.5%, 10%) across a 1-h time-course. Each of these agonists significantly increased sucrose intake with variations in pattern, magnitude, and consistency as a function of sucrose concentration. Whereas the mu opioid agonist, DAMGO, and the delta, opioid agonist, DPDPE, each enhanced sucrose intake at higher (2.5%, 10%), but not lower (0.5%), concentrations, the delta(2) opioid agonist, DeIt II, increased sucrose intake at lower (0.5%, 2.5%, 2.5%), but not higher (10%), concentrations. Kappa opioid agonists produced less consistent effects. The kappa(1) opioid agonist, U50488H, increased sucrose intake at high (10%) concentrations and decreased sucrose intake at low (0.5%) concentrations, and the kappa(3) opioid agonist, NalBzOH, inconsistently increased sucrose intake at the 0.5% (20 mu g) and 10% (1 mu g) concentrations. Thus, these data further implicate mu, delta(1), and delta(2) opioid mediation of palatable intake, particularly of its orosensory characteristics. (C) 1997 Elsevier Science Inc.