Abstract
BackgroundIn this paper, we reviewed translational studies concerned with environmental influences on the rewarding effects of heroin versus cocaine in rats and humans with substance use disorder. These studies show that both experienced utility (‘liking’) and decision utility (‘wanting’) of heroin and cocaine shift in opposite directions as a function of the setting in which these drugs were used. Briefly, rats and humans prefer using heroin at home but cocaine outside the home. These findings appear to challenge prevailing theories of drug reward, which focus on the notion of shared substrate of action for drug of abuse, and in particular on their shared ability to facilitate dopaminergic transmission.AimsThus, in the second part of the paper, we verified whether our findings could be accounted for by available computational models of reward. To account for our findings, a model must include a component that could mediate the substance-specific influence of setting on drug rewardResultsIt appears of the extant models that none is fully compatible with the results of our studies.ConclusionsWe hope that this paper will serve as stimulus to design computational models more attuned to the complex mechanisms responsible for the rewarding effects of drugs in real-world contexts.
Highlights
ConclusionsWe hope that this paper will serve as stimulus to design computational models more attuned to the complex mechanisms responsible for the rewarding effects of drugs in real-world contexts
It is well known that, under certain conditions, some individuals eagerly self-administer drugs such as heroin and cocaine
We will first review translational studies showing that the setting of drug use can influence in opposite directions the rewarding effects of opioids versus psychostimulants in rats and humans
Summary
We have reviewed here a series of translational studies demonstrating that the experienced utility and decision utility of heroin and cocaine are modulated in opposite direction by the circumstances of drug use. We have shown that with some tweaking the architecture of the Michigan model (Robinson and Berridge 1993; Berridge 2012) and its computational version (Zhang et al 2009; Dayan and Berridge 2014) can accommodate most of our findings, except for the critical role that this model attributes to dopamine In this respect, it is worth noticing that in the graphic representations of the Michigan model, no specific neurobiological label is attached to its components, including the incentive salience attributor (e.g., Figure 2 in Robinson and Berridge 1993, and Figure 1 in Berridge 2012; but see Figure 1 in Berridge and Robinson 2016). 275): “Regardless, we want to emphasize that the Incentive-Sensitization Theory of Addiction does not require that the sole or even primary site of drug-induced neuroadaptations responsible for craving be on dopamine neurons. We hope that this paper will serve as stimulus to design computational models more attuned to the complex mechanisms responsible for the rewarding effects of drugs in real-world contexts
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