Fiancette, J.F Simonnet, A. Courtin, J. Renault, P. Piazza, PV. Deroche-‐Gamonet, .V Herry, C
INSERM U862, Neurocentre Magendie, Bordeaux-‐F33077, France
Cocaine addiction is a psychiatric condition defined as compulsive drug taking despite severe negative consequences for the user. It occurs after prolonged drug use in about 20% of cocaine users. We developed a rat model that closely mimics this vulnerability to lose control over cocaine use with 15-‐20% of the rats displaying the behavioral hallmarks of addiction after prolonged cocaine self-‐administration. This animal model provides excellent face and predictive validities and is a necessary prerequisite for studying the pathophysiological mechanisms of addictive behavior. From a functional standpoint, evidence suggest that distinct, but interconnected circuits, including the nucleus accumbens (NAc), the medial prefrontal cortex (mPFC) and basolateral amygdala (BLA) are at the core of pathological incentive processes and difficulties to control drug taking. However the functional interactions that occur between these neuronal structures during cocaine addiction are poorly understood. To further address this question, we performed simultaneous single unit and local field potential recordings in NAc, mPFC and BLA in rats behaviorally characterized as addicted or non-‐addicted-‐like after 3 months of cocaine self-‐administration. Our results indicate a reduced functional connectivity between these neuronal structures in addicted compared to non-‐addicted-‐like rats, as assessed by local and long-‐range neuronal correlations. These preliminary results support the notion that cocaine addiction is associated with functional alterations of specific neuronal circuits and could further provide, in part, an explanation of the individual differences in vulnerability to cocaine addiction.