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When chocolate seeking becomes compulsion: gene-environment interplay.

Patrono E, Di Segni M, Patella L, Andolina D, Valzania A, Latagliata EC, Felsani A, Pompili A, Gasbarri A, Puglisi-Allegra S, Ventura R - PLoS ONE (2015)

Bottom Line: This behavioral pattern is linked to decreased availability of accumbal D2R.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Applied Clinical Science and Biotechnology, University of L'Aquila, Coppito, Italy.

ABSTRACT

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 α1R 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 α1R 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.

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Related in: MedlinePlus

Conditioned Suppression Training in C57 and DBA mice.Time spent (sec ± SE) in the chamber containing chocolate (C-C) and in the empty safe chamber (ES-C) during training phase by Control C57/DBA groups (n = 6 for each group) (A) and Stressed C57/DBA mice (n = 8 for each group) (B). * p< 0.05 in comparison with ES-C.
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pone.0120191.g002: Conditioned Suppression Training in C57 and DBA mice.Time spent (sec ± SE) in the chamber containing chocolate (C-C) and in the empty safe chamber (ES-C) during training phase by Control C57/DBA groups (n = 6 for each group) (A) and Stressed C57/DBA mice (n = 8 for each group) (B). * p< 0.05 in comparison with ES-C.

Mentions: In the analysis of the training phase, we observed a significant strain x treatment x chamber interaction (F(1,72) = 6.52; p< 0.001). Comparison of the time spent in the C-C and ES-C in each group indicated that only the Control C57 and Stressed DBA groups preferred the C-C versus the ES-C during the training phase (Control C57: F(1,10) = 6.32; p< 0.05; Stressed DBA: F(1,14) = 15.60; p< 0.05) (Fig. 2), spending more time in the C-C than ES-C.


When chocolate seeking becomes compulsion: gene-environment interplay.

Patrono E, Di Segni M, Patella L, Andolina D, Valzania A, Latagliata EC, Felsani A, Pompili A, Gasbarri A, Puglisi-Allegra S, Ventura R - PLoS ONE (2015)

Conditioned Suppression Training in C57 and DBA mice.Time spent (sec ± SE) in the chamber containing chocolate (C-C) and in the empty safe chamber (ES-C) during training phase by Control C57/DBA groups (n = 6 for each group) (A) and Stressed C57/DBA mice (n = 8 for each group) (B). * p< 0.05 in comparison with ES-C.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4363151&req=5

pone.0120191.g002: Conditioned Suppression Training in C57 and DBA mice.Time spent (sec ± SE) in the chamber containing chocolate (C-C) and in the empty safe chamber (ES-C) during training phase by Control C57/DBA groups (n = 6 for each group) (A) and Stressed C57/DBA mice (n = 8 for each group) (B). * p< 0.05 in comparison with ES-C.
Mentions: In the analysis of the training phase, we observed a significant strain x treatment x chamber interaction (F(1,72) = 6.52; p< 0.001). Comparison of the time spent in the C-C and ES-C in each group indicated that only the Control C57 and Stressed DBA groups preferred the C-C versus the ES-C during the training phase (Control C57: F(1,10) = 6.32; p< 0.05; Stressed DBA: F(1,14) = 15.60; p< 0.05) (Fig. 2), spending more time in the C-C than ES-C.

Bottom Line: This behavioral pattern is linked to decreased availability of accumbal D2R.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Applied Clinical Science and Biotechnology, University of L'Aquila, Coppito, Italy.

ABSTRACT

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 α1R 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 α1R 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.

Show MeSH
Related in: MedlinePlus