Naltrexone administered to central nucleus of amygdala or PVN: neural dissociation of diet and energy.

There is evidence that opioids may affect food consumption through mechanisms as diverse as reward or energy metabolism. However, these hypotheses are derived from studies employing peripheral or, more rarely, intracerebroventricular administration of drugs. Opioid receptors have a wide distribution in the central nervous system and include a number of regions implicated in food intake such as the hypothalamic paraventricular nucleus (PVN) and the central nucleus of the amygdala (ACe). It is not known whether local opioid receptor blockade in either of these regions will produce similar effects on food intake. To examine this issue, a chronic cannula was aimed at either the PVN or ACe of rats that were fed a choice of a high-fat and high-carbohydrate diet, which allows for the measurement of both preference and total energy consumption. Naltrexone influenced preferred and nonpreferred food consumption, depending on the site of administration. Consumption of both preferred and nonpreferred diets was suppressed after PVN naltrexone administration, whereas only preferred diet intake was reduced after ACe injection of naltrexone. The present evidence indicates that direct stimulation of different brain regions with naltrexone may be associated with diverse effects on diet selection, which may be accounted for by manipulation of specific functional neural circuitry.