Central opioid receptor subtype antagonists differentially alter sucrose and deprivation-induced water intake in rats.

The present study compared the effectiveness of centrally-administered opioid receptor subtype antagonists to inhibit intake of either a 10% sucrose solution under ad libitum conditions, or water following 24 h of water deprivation. Full dose-response functions were evaluated over a 1 h period for the following antagonists: naltrexone (general: 1-50 micrograms), nor-binaltorphamine (Nor-BNI, kappa: 1-20 micrograms), beta-funaltrexamine (beta-FNA, mu: 1-20 micrograms), naltrindole (delta 2: 1-20 micrograms), [D-Ala2, Leu5, Cys6]-enkephalin (DALCE, delta 1: 10-40 micrograms) and naloxonazine (mu 1: 10-50 micrograms). Naltrexone significantly and dose-dependently inhibited both sucrose intake (64-67%) and deprivation-induced water intake (53-67%). Nor-BNI significantly and dose-dependently inhibited sucrose intake (53-55%), but failed to significantly affect (28%) deprivation-induced water intake. beta-FNA significantly and dose-dependently inhibited both sucrose intake (31-34%) and deprivation-induced water intake (36-50%). Naltrindole failed to significantly alter either sucrose intake (24%) or deprivation-induced water intake (16%). Whereas DALCE significantly, but transiently (15-20 min) inhibited sucrose intake (28%), it failed to significantly alter deprivation-induced water intake (14%). Naloxonazine significantly, but transiently (5-10 min) stimulated sucrose intake at low doses (26%), but non-significantly reduced sucrose intake at higher doses (20%). Naloxonazine failed to significantly alter deprivation-induced water intake (16% reduction). These data indicate that whereas the kappa and mu 2 binding sites participate in the opioid modulation of sucrose intake, the mu 2 binding site participates in the opioid modulation of deprivation-induced water intake.