Abstract
Highly palatable foods and dieting are major contributing factors for the development of compulsive eating in obesity and eating disorders. We previously demonstrated that intermittent access to palatable food results in corticotropin-releasing factor-1 (CRF1) receptor antagonist-reversible behaviors, which include excessive palatable food intake, hypophagia of regular chow, and anxiety-like behavior. However, the brain areas mediating these effects are still unknown. Male Wistar rats were either fed chow continuously for 7 days/week (Chow/Chow group), or fed chow intermittently 5 days/week, followed by a sucrose, palatable diet 2 days/week (Chow/Palatable group). Following chronic diet alternation, the effects of microinfusing the CRF1 receptor antagonist R121919 (0, 0.5, 1.5 μg/side) in the central nucleus of the amygdala (CeA), the basolateral nucleus of the amygdala (BlA), or the bed nucleus of the stria terminalis (BNST) were evaluated on excessive intake of the palatable diet, chow hypophagia, and anxiety-like behavior. Furthermore, CRF immunostaining was evaluated in the brain of diet cycled rats. Intra-CeA R121919 blocked both excessive palatable food intake and anxiety-like behavior in Chow/Palatable rats, without affecting chow hypophagia. Conversely, intra-BlA R121919 reduced the chow hypophagia in Chow/Palatable rats, without affecting excessive palatable food intake or anxiety-like behavior. Intra-BNST treatment had no effect. The treatments did not modify the behavior of Chow/Chow rats. Immunohistochemistry revealed an increased number of CRF-positive cells in CeA—but not in BlA or BNST—of Chow/Palatable rats, during both withdrawal and renewed access to the palatable diet, compared with controls. These results provide functional evidence that the CRF–CRF1 receptor system in CeA and BlA has a differential role in mediating maladaptive behaviors resulting from palatable diet cycling.
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Acknowledgements
We thank Duncan Momaney, Aditi R Narayan, Jina Kwak for technical assistance, and Tamara Zeric for technical and editorial assistance. We also thank Elena F Crawford for helpful suggestions related to CRF immunohistochemistry. This publication was made possible by grant numbers DA023680, DA030425, MH091945, MH093650, and AA016731, from the National Institute on Drug Abuse (NIDA), the National Institute of Mental Health (NIMH), and the National Institute on Alcohol Abuse and Alcoholism (NIAAA), by the Peter Paul Career Development Professorship (PC) and by Boston University's Undergraduate Research Opportunities Program (UROP). This research was also supported by the NIH Intramural Research Programs of the National Institute on Drug Abuse, and the National Institute of Alcohol Abuse and Alcoholism, NIH, DHHS. Its contents are solely the responsibility of the authors and do not necessarily represent the official views of the National Institutes of Health.
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Iemolo, A., Blasio, A., St Cyr, S. et al. CRF–CRF1 Receptor System in the Central and Basolateral Nuclei of the Amygdala Differentially Mediates Excessive Eating of Palatable Food. Neuropsychopharmacol 38, 2456–2466 (2013). https://doi.org/10.1038/npp.2013.147
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DOI: https://doi.org/10.1038/npp.2013.147
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