Alterations in deprivation, glucoprivic and sucrose intake following general, mu and kappa opioid antagonists in the hypothalamic paraventricular nucleus of rats

• Published in: Neuroscience Vol. 66; no. 4; pp. 951 - 957
• Main Authors: Koch, J.E., Glass, M.J., Cooper, M.L., Bodnar, R.J.
• Format: Journal Article
• Language: English
• Published: Oxford Elsevier Ltd 01.06.1995; Elsevier
• Subjects: 2-deoxy- d-glucose; 2-DG; Animals; beta-funaltrexamine (mu opioid antagonist); Biological and medical sciences; Eating; Feeding. Feeding behavior; Food Deprivation; Fundamental and applied biological sciences. Psychology; Hypothalamus - drug effects; Male; Naltrexone - analogs & derivatives; Naltrexone - pharmacology; Nor-BNI; norbinaltorphamine (kappa opioid antagonist); Paraventricular Hypothalamic Nucleus - drug effects; paraventricular nucleus; PVN; Rats; Rats, Sprague-Dawley; Receptors, Opioid, kappa - antagonists & inhibitors; Receptors, Opioid, mu - antagonists & inhibitors; Sucrose; Vertebrates: anatomy and physiology, studies on body, several organs or systems; β-FNA; β-FNA; 2-DG; beta-funaltrexamine (mu opioid antagonist); PVN; Nor-BNI; norbinaltorphamine (kappa opioid antagonist); 2-deoxy- d-glucose; paraventricular nucleus; Vertebrata; Mammalia; Rat; Food intake; Rodentia; Central nervous system; Antagonist; Hypothalamus; Paraventricular nucleus; Opiate receptor μ; Brain (vertebrata); Opiate receptor κ
• ISSN: 0306-4522; 1873-7544
• DOI: 10.1016/0306-4522(95)00001-Y

While opioid agonists administered into the hypothalamic paraventricular nucleus increase food intake in rats, naloxone reduces deprivation-induced intake. Ventricular administration of either mu (beta-funaltrexamine) or kappa (nor-binaltorphamine) opioid antagonists reduces spontaneous, deprivation, glucoprivic and palatable intake. The present study assessed whether microinjections of either general, mu or kappa opioid antagonists into the paraventricular nucleus altered either deprivation (24 h) intake, 2-deoxy- d-glucose hyperphagia or sucrose intake in rats. Deprivation intake was significantly reduced by nor-binaltorphamine (5 μg, 68 nmol, 30–33%), beta-funaltrexamine (5 μg, 100 nmol, 26–29%) or naltrexone (10 μg, 260 nmol, 26%) in the paraventricular nucleus. 2-Deoxy- d-glucose hyperphagia was significantly reduced only after 2 h by naltrexone (10 μg, 260 nmol, 69%), norbinaltorphamine (20 μg, 272 nmol, 69%) or beta-funaltrexamine (20 μg, 400 nmol, 83%) in the paraventricular nucleus. Sucrose intake was significantly reduced by nor-binaltorphamine (5 μg, 68 nmol, 27–36%), naltrexone (5–10 μg, 130–260 nmol, 18–31%) and beta-funaltrexamine (5 μg, 100 nmol, 20%) in the paraventricular nucleus. These data indicate that general, mu and kappa opioid antagonists administered into the hypothalamic paraventricular nucleus produce similar patterns of effects upon different forms of food intake as did ventricular administration, implicating this nucleus as part of the circuitry underlying opioid mediation of ingestion.