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 micrograms, 68 nmol, 30-33%),
beta-funaltrexamine (5 micrograms, 100 nmol, 26-29%) or
naltrexone (10 micrograms, 260 nmol, 26%) in the paraventricular nucleus.
2-Deoxy-D-glucose hyperphagia was significantly reduced only after 2 h by
naltrexone (10 micrograms, 260 nmol, 69%), norbinaltorphamine (20 micrograms, 272 nmol, 69%) or
beta-funaltrexamine (20 micrograms, 400 nmol, 83%) in the paraventricular nucleus.
Sucrose intake was significantly reduced by nor-binaltorphamine (5 micrograms, 68 nmol, 27-36%),
naltrexone (5-10 micrograms, 130-260 nmol, 18-31%) and
beta-funaltrexamine (5 micrograms, 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.