The neuroscience of addiction
National Institute on Drug Abuse, USA.Nature Neuroscience (Impact Factor: 14.98). 12/2005; 8(11):1429-30. DOI: 10.1038/nn1105-1429
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ABSTRACT: "Food addiction" is an emerging area, and behavioral and biological overlaps have been observed between eating and addictive disorders. Potential misconceptions about applying an addiction framework to problematic eating behavior may inhibit scientific progress. Critiques of "food addiction" that focus on descriptive differences between overeating and illicit drugs are similar to early criticisms of the addictiveness of tobacco. Although food is necessary for survival, the highly processed foods associated with addictive-like eating may provide little health benefit. Individual differences are important in determining who develops an addiction. If certain foods are addictive, the identification of possible risk factors for "food addiction" is an important next step. Not all treatments for addiction require abstinence. Addiction interventions that focus on moderation or controlled use may lead to novel approaches to treating eating-related problems. Finally, addiction-related policies that focus on environmental (instead of educational) targets may have a larger public health impact in reducing overeating.Current Psychiatry Reports 04/2015; 17(4):563. DOI:10.1007/s11920-015-0563-3 · 3.05 Impact Factor
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ABSTRACT: 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. 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 α 1R levels in the medial prefrontal cortex, respectively, by western blot. 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 α 1R 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 α1R downregulation in the striatum and medial prefrontal cortex, respectively, are potential neuroadaptive responses that parallel the shift from motivated to compulsive eating.PLoS ONE 03/2015; 10(3). DOI:10.1371/journal.pone.0120191 · 3.53 Impact Factor
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