Physiological correlates of cocaine addition

Sandra Helinski

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.