Abstract
Individuals suffering from substance use disorders often show severely impaired social interaction, preferring drugs of abuse to the contact with others. Their impaired social interaction is doubly harmful for them as (1) therapy itself is based and dependent on social interaction and as (2) social interaction is not available to them as an “alternative”, i.e., non-drug reward, decreasing their motivation to stop drug use. We therefore developed an animal experimental model to investigate the neurobiology of dyadic social interaction- vs. cocaine reward. We took care to avoid: (a) engaging sexual attraction-related aspects of such a social interaction and (b) hierarchical difference as confounding stimuli. The cocaine- or social interaction stimulus was offered – in a mutually exclusive setting – within the confines of a conditioned place preference (CPP) apparatus. In our paradigm, only four 15-min episodes of social interaction proved sufficient to (i) switch the rats’ preference from cocaine-associated contextual stimuli to social interaction CPP and (ii) inhibit the subsequent reacquisition/reexpression of cocaine CPP. This behavioral effect was paralleled by a reversal of brain activation (i.e., EGR1 expression) in the nucleus accumbens, the central and basolateral amygdala, and the ventral tegmental area. Of relevance for the psychotherapy of addictive disorders, the most rewarding sensory component of the composite stimulus “social interaction” was touch. To test our hypothesis that motivation is encoded in neuron ensembles dedicated to specific reward scenarios, we are currently (1) mapping the neural circuits involved in cocaine- vs. social-interaction reward and (2) adapting our paradigm for C57BL/6 mice to make use of the plethora of transgenic models available in this species.
Highlights
Individuals suffering from substance use disorders often show severely impaired social interaction, preferring drugs of abuse to the contact with others
The results were very encouraging, robust, and have so far been demonstrated by three generations of experimenters comprising a total of seven individual experimenters [3,4,5,6]: just four episodes of 15-min dyadic social interaction (DSI) with a weight- and sex-matched male conspecific were able to countercondition place preference from cocaine to this form of social interaction but, following a subsequent cocaine exposure, were able to inhibit the reacquisition of cocaine conditioned place preference (CPP) that regularly occurred if the rats’ cocaine CPP was extinguished without social interaction counterconditioning (SIC)
The behavioral reversal was paralleled by a DSImediated reversal in the cocaine CPP-induced activation of several brain regions implicated in reward/reinforcement: the nucleus accumbens shell (AcbSh) and core (AcbC), the central (CeA) and basolateral (BLA) amygdala, and the ventral tegmental area (VTA)
Summary
Individuals suffering from substance use disorders often show severely impaired social interaction, preferring drugs of abuse to the contact with others. Their impaired social interaction is doubly harmful for them as [1] therapy itself is based and dependent on social interaction with their psychotherapist [1, 2], physician, case manager, etc., and as [2] social interaction is not available to them as an “alternative”, i.e., non-drug reward, decreasing their motivation to stop drug use. A number of patients suffering from a variety of psychiatric disorders would profit from the societally beneficial investigation of the neurobiological basis of the shift of one’s preference from a harmful stimulus to social interaction
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