On a neuronal level, addicted behavior is characterized by an intense stimulation of the mesolimbic-mesocortical dopaminergic reward system. This dopaminergic stimulation enhances target-oriented behavior to repeatedly obtain the rewarding substance. Incremental neuroadaptations occur during long-term use of this substance, resulting in a dysfunctional reward system. For instance, addicted people show lower reactivity to natural reinforcers that are unrelated to the substance. Our research focuses on the investigation of possible deficits in such reward-dependent functions, especially implicit vs. explicit reward learning. We investigate reward-dependent learning in relation to present addictive behavior to different substances (e.g. nicotine, alcohol and relevant sub-groups like binge drinkers) and other rewarding behaviors (e.g. shopping, eating) as well as possible moderators on the reward system (e.g. satiation, depression). We are also interested in the fact if a deficient reward system is the cause or the consequence of addictive behavior.
Other disorders like bulimia nervosa, binge eating disorder or obesity are often compared to addiction. Eating behavior and addiction show similar short- and long-term neuronal mechanisms in the reward system. Addiction-related stimuli lead to an overactivation of motivational- and approach-networks in addicted people, accompanied by an impaired activation of inhibitory neuronal structures (Fig. 1). Therefore, another project investigates if the construct “food addiction” is valid, how it can be assessed and if eating disordered people show similar peripheral, psychological and neuronal reactions, when they are confronted with disorder-related stimuli like addicted patients do in substance dependence.