Individuals suffering from substance use disorders often show severely impaired social interaction, old taylor whiskey 1933 price 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 copyright 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 copyright- 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 copyright-associated contextual stimuli to social interaction CPP and (ii) inhibit the subsequent reacquisition/reexpression of copyright CPP.The 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 copyright- vs social interaction 9002nc reward and (2) adapting our paradigm for C57BL/6 mice to make use of the plethora of transgenic models available in this species.