The role of the amygdala in palatability and homeostatic models of high-fat feeding
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[ACCESS RESTRICTED TO THE UNIVERSITY OF MISSOURI AT AUTHOR'S REQUEST.] Previous research has demonstrated a dissociation of certain neural mediators that contribute to the increased consumption of a high-fat diet following intra-accumbens (Acb) administration of ?-opioid receptor agonists vs. 24-hr food deprivation. The focus of this research is to explore this distributed network of the amygdala, nucleus accumbens, and other limbic system structures and the endogenous opioid systems therein that contribute to these two distinct feeding types. The present experiments were conducted to examine the more specific role of CeA and BLA opioid transmission in mediating high-fat feeding driven by either intra-Acb administration of the ?-opioid agonist D-Ala2-NMe-Phe4-Glyol5-enkephalin (DAMGO) or 24-hr home cage food deprivation. Injection of DAMGO into the Acb (0.25 ?g/.5?l/side) increased consumption of the high-fat diet, and consumption was reduced by BLA administration of the opioid antagonist, naltrexone (5?g/.25?l/side). In contrast, intra-CeA naltrexone administration had no effect on high-fat intake driven by intra-Acb DAMGO. Meanwhile, intra-CeA naltrexone administration blocked increased high fat consumption following 24-hr food deprivation, demonstrating a specific role for CeA opioid transmission in high-fat consumption. As expected, intra-BLA naltrexone administration had no effect on high-fat feeding following 24-hour food deprivation. Neither intra-CeA nor intra-BLA naltrexone administration alone had a significant effect on baseline feeding levels within either feeding model. These findings suggest that CeA opioid transmission mediates consumption of a palatable high-fat diet driven by short-term negative-energy balance (24-hr food deprivation), while BLA opioid transmission is mediates consumption following intra-Acb opioid receptor activation.
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