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Publication : When chocolate seeking becomes compulsion: gene-environment interplay.

First Author  Patrono E Year  2015
Journal  PLoS One Volume  10
Issue  3 Pages  e0120191
PubMed ID  25781028 Mgi Jnum  J:229202
Mgi Id  MGI:5751036 Doi  10.1371/journal.pone.0120191
Citation  Patrono E, et al. (2015) When chocolate seeking becomes compulsion: gene-environment interplay. PLoS One 10(3):e0120191
abstractText  BACKGROUND: Eating disorders appear to be caused by a complex interaction between environmental and genetic factors, and compulsive eating in response to adverse circumstances characterizes many eating disorders. MATERIALS AND METHODS: We compared compulsion-like eating in the form of conditioned suppression of palatable food-seeking in adverse situations in stressed C57BL/6J and DBA/2J mice, two well-characterized inbred strains, to determine the influence of gene-environment interplay on this behavioral phenotype. Moreover, we tested the hypothesis that low accumbal D2 receptor (R) availability is a genetic risk factor of food compulsion-like behavior and that environmental conditions that induce compulsive eating alter D2R expression in the striatum. To this end, we measured D1R and D2R expression in the striatum and D1R, D2R and alpha1R levels in the medial prefrontal cortex, respectively, by western blot. RESULTS: Exposure to environmental conditions induces compulsion-like eating behavior, depending on genetic background. This behavioral pattern is linked to decreased availability of accumbal D2R. Moreover, exposure to certain environmental conditions upregulates D2R and downregulates alpha1R in the striatum and medial prefrontal cortex, respectively, of compulsive animals. These findings confirm the function of gene-environment interplay in the manifestation of compulsive eating and support the hypothesis that low accumbal D2R availability is a "constitutive" genetic risk factor for compulsion-like eating behavior. Finally, D2R upregulation and alpha1R downregulation in the striatum and medial prefrontal cortex, respectively, are potential neuroadaptive responses that parallel the shift from motivated to compulsive eating.
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