Basolateral amygdala opioids contribute to increased high-fat intake following intra-accumbens opioid administration, but not following 24-h food deprivation

Previous research has demonstrated that administration of p-opioid receptor agonists into the nucleus accumbens increases high-fat diet consumption in sated rats and has shown a role of basolateral amygdala (BLA) activity in mediating this response. The present experiments were conducted to examine the role of BLA opioid transmission in mediating high-fat feeding driven by either intra-accumbens opioid activation or 24-h home cage food deprivation. Injection of the p-opioid agonist, D-Ala2-NMe-Phe4-Glyol5-enkephalin (DAMGO) into the nucleus accumbens (0.25 mu g/0.5 mu l/side) increased consumption of a high-fat diet, and this effect was attenuated by pre-treatment with the opioid antagonist, naltrexone (5 mu g/0.25 mu 1/side) administered into the BLA. In contrast, intra-BLA naltrexone administration had no influence on the increase in high-fat intake following 24-h food deprivation. These findings suggest that BLA opioid transmission is an important mediator of palatability-driven feeding as modeled by intra-accumbens opioid activation, while BLA opioid transmission has no significant influence on the increase in high-fat feeding driven by short-term negative-energy balance. (C) 2010 Elsevier Inc. All rights reserved.