Intake of either hypotonic or hypertonic saline solutions is modulated in part by the endogenous opioid system. Morphine and selective mu and delta opioid agonists increase saline intake, while general opioid antagonists reduce saline intake in rats. The present study evaluated whether intracerebroventricular administration of general (naltrexone) and selective mu (beta-funaltrexamins, 5–20 μg), mu 1 (naloxonazine, 50 μg), kappa (nor-binaltorphamine, 5–20 μg), delta (naltrindole, 20 μg), or delta, (DALCE, 40 μg) opioid receptor subtype antagonists altered water intake and either hypotonic (0.6%) or hypertonic (1.7%) saline intake in water-deprived (24 h) rats over a 3-h time course in a two-bottle choice test. Whereas peripheral naltrexone (0.5–2.5 mg/kg) significantly reduced water intake and hypertonic saline intake, central naltrexone (1–50 μg) significantly reduced water intake and hypotonic saline intake. Water intake was significantly reduced following mu and kappa receptor antagonism, but not following mu 1 , delta, or delta 1 receptor antagonism. In contrast, neither hypotonic nor hypertonic saline intake was significantly altered by any selective antagonist. These data are discussed in terms of opioid receptor subtype control over saline intake relative to the animal's hydrational state and the roles of palatability and/or salt appetite.
Brain Research Bulletin – Elsevier
Published: Jan 1, 1995
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