That is because many experiments use systemic drug administration, genetic manipulations or neural sensitization to alter reward, and all are bound to impact many dopamine systems simultaneously. This discussion centers on mesolimbic dopamine projections especially to nucleus accumbens, but in practice, it is often difficult to distinguish the role of mesolimbic dopamine from neostriatal, cortical, and other dopamine systems. Thus, dopamine deserves the special attention it has received as a crucial node of reward, and its precise role needs to be understood.Īnatomical caveat. Still, many causal manipulations powerfully affect reward by acting directly or indirectly on dopamine neurotransmission, and dopamine neural activation clearly codes reward events. Dopamine is just one link in that chain of neuronal signals, and of course, we must go beyond dopamine neurons and synapses to understand reward function.

In this paper, ‘the role of dopamine in reward’ is taken to be a short-hand term for the dopaminergic component of mesocorticolimbic systems. In short, dopamine’s contribution appears to be chiefly to cause ‘wanting’ for hedonic rewards, more than ‘liking’ or learning for those rewards.īeyond dopamine caveat.

Results from studies that exploited those opportunities are described here. That interaction sets the stage to cause compulsive ‘wanting’ in addiction, but also provides opportunities for experiments to disentangle ‘wanting’, ‘liking’, and learning hypotheses. Such drugs interact with incentive salience integrations of Pavlovian associative information with physiological state signals. Drugs of abuse that promote dopamine signals short circuit and sensitize dynamic mesolimbic mechanisms that evolved to attribute incentive salience to rewards. Dopamine appears necessary for normal ‘wanting’, and dopamine activation can be sufficient to enhance cue-triggered incentive salience. By contrast, growing evidence indicates that dopamine does contribute causally to incentive salience. Other recent evidence indicates that dopamine is not needed for new learning, and not sufficient to directly mediate learning by causing teaching or prediction signals. In brief, recent evidence indicates that dopamine is neither necessary nor sufficient to mediate changes in hedonic ‘liking’ for sensory pleasures.

Does dopamine mostly mediate the hedonic impact of reward (‘liking’)? Does it instead mediate learned predictions of future reward, prediction error teaching signals and stamp in associative links (learning)? Or does dopamine motivate the pursuit of rewards by attributing incentive salience to reward-related stimuli (‘wanting’)? Each hypothesis is evaluated here, and it is suggested that the incentive salience or ‘wanting’ hypothesis of dopamine function may be consistent with more evidence than either learning or ‘liking’. There are three competing explanatory categories: ‘liking’, learning, and ‘wanting’. Debate continues over the precise causal contribution made by mesolimbic dopamine systems to reward.

Hedonic tonic