Behavioral Characterization of Amygdala Involvement in Mediating Intra-Accumbens Opioid-Driven Feeding Behavior.

The present experiments were conducted to provide a more detailed behavioral analysis of the dissociable roles of the basolateral (BLA) and central nucleus (CeA) of the amygdala in mediating intra-accumbens (Acb) opioid-induced Feeding of a high-fat diet. Confirming previous findings, temporary inac...

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Detalles Bibliográficos
Publicado en:Behavioral Neuroscience Vol. 123; no. 4; pp. 781 - 794
Autores principales: Will, Matthew J., Pritchett, Carolyn E., Parker, Kyle E.
Formato: Artículo
Publicado: American Psychological Association August 2009
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Acceso en línea:Ver este registro en EBSCOhost
Descripción
Sumario:The present experiments were conducted to provide a more detailed behavioral analysis of the dissociable roles of the basolateral (BLA) and central nucleus (CeA) of the amygdala in mediating intra-accumbens (Acb) opioid-induced Feeding of a high-fat diet. Confirming previous findings, temporary inactivalion of the CeA with the GABAA agonist muscimol reduced DAMGO (D-Ala2-NMe-Phe4-Glyol5-enkephalin)-induced and baseline food intake, whereas intra-BLA muscimol selectively blocked only DAMGO-induced food intake, leaving baseline feeding intact. However, although inactivation of the BLA reduced DAMGO-induced food intake to control levels, this treatment led to exaggerated number and duration of food hopper entries after food intake had ended. A subsequent experiment under conditions of limited access to the diet found the identical pattern of behavior following intra-Acb administration of DAMGO, regardless of whether the BLA was inactivated. Last, BLA inactivation was shown to have no influence on feeding driven by a state of negative-energy balance (24-hr food deprivation), demonstrating a specific-influence of the BLA on opioid-driven feeding. These findings suggest that BLA mediates palatability-driven feeding and that this influence is particular to the consummatory act of ingestion. Reprinted by permission of the publisher.