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Neurobiological bases of eating addictive-like behavior| old_uid | 16631 |
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| title | Neurobiological bases of eating addictive-like behavior |
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| start_date | 2018/10/26 |
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| schedule | 11h |
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| online | no |
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| location_info | salle B501 |
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| summary | An increasing perspective conceptualizes obesity and overeating as disorders related to addictive- like processes that could share common neurobiological mechanisms. We aimed at validating an animal model of eating addictive-like behavior in mice, based on the DSM-5 substance use disorder criteria, using operant conditioning maintained by highly palatable chocolate-flavored pellets. For this purpose, we evaluated persistence of food-seeking during a period of non-availability of food, motivation for food, and perseverance of responding when the reward was associated with a punishment. This model has allowed identifying extreme subpopulations of mice related to addictive-like behavior. We investigated in these subpopulations the Epigenetic and proteomic studies have allowed to identify a significant decrease in DNA methylation of CNR1 gene promoter in the prefrontal cortex of addict-like mice, which was associated with an upregulation of CB1 protein expression in the same brain area. The pharmacological blockade of CB1 receptor during the late training period reduced the percentage of mice that accomplished addiction criteria, which is in agreement with the reduced performance of CB1 knockout mice in this operant training. Proteomic studies have identified proteins differentially expressed in mice vulnerable or not to addictive-like behavior in the hippocampus, striatum, and prefrontal cortex. The use of DREADD techniques in this model has now allowed identifying the crucial role of the prefrontal cortex in the development of eating addictive-like behavior. This model provides an excellent tool to investigate the neurobiological mechanisms underlying eating addictive-like behavior. |
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| responsibles | Tratner |
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