What is the role of dopamine in reward: hedonic impact, reward learning, or incentive salience?

• Published in: Brain Research Reviews 1998-12, Vol.28 (3), p.309-369
• Main Authors: Berridge, Kent C, Robinson, Terry E
• Format: Article
• Language: English
• Subjects: 6-hydroxydopamine; Addiction; Affect; Anhedonia; Aphagia; Appetite; Aversion; Behavioral psychophysiology; Biological and medical sciences; Brain; Conditioned taste aversion; Conditioning; Consummatory behavior; Diazepam; Dopamine; Emotion; Feeding; Food intake appetitive behavior; Fundamental and applied biological sciences. Psychology; Hedonic; Ingestion; Lateral hypothalamus; Mesolimbic; Mesotelencephalic mesostriatal; Motivation; Neostriatum; Neurotransmission and behavior; Neurotransmitters; Nigrostriatal; Nucleus accumbens; Palatability; Pleasure; Psychology. Psychoanalysis. Psychiatry; Psychology. Psychophysiology; Reinforcement; Reward; Self-administration; Substance-related disorders; Substantia nigra; Taste; Taste reactivity; Tegmentum
• ISSN: 0165-0173; 1872-6321
• DOI: 10.1016/S0165-0173(98)00019-8

What roles do mesolimbic and neostriatal dopamine systems play in reward? Do they mediate the hedonic impact of rewarding stimuli? Do they mediate hedonic reward learning and associative prediction? Our review of the literature, together with results of a new study of residual reward capacity after dopamine depletion, indicates the answer to both questions is `no'. Rather, dopamine systems may mediate the incentive salience of rewards, modulating their motivational value in a manner separable from hedonia and reward learning. In a study of the consequences of dopamine loss, rats were depleted of dopamine in the nucleus accumbens and neostriatum by up to 99% using 6-hydroxydopamine. In a series of experiments, we applied the `taste reactivity' measure of affective reactions (gapes, etc.) to assess the capacity of dopamine-depleted rats for: 1) normal affect (hedonic and aversive reactions), 2) modulation of hedonic affect by associative learning (taste aversion conditioning), and 3) hedonic enhancement of affect by non-dopaminergic pharmacological manipulation of palatability (benzodiazepine administration). We found normal hedonic reaction patterns to sucrose vs. quinine, normal learning of new hedonic stimulus values (a change in palatability based on predictive relations), and normal pharmacological hedonic enhancement of palatability. We discuss these results in the context of hypotheses and data concerning the role of dopamine in reward. We review neurochemical, electrophysiological, and other behavioral evidence. We conclude that dopamine systems are not needed either to mediate the hedonic pleasure of reinforcers or to mediate predictive associations involved in hedonic reward learning. We conclude instead that dopamine may be more important to incentive salience attributions to the neural representations of reward-related stimuli. Incentive salience, we suggest, is a distinct component of motivation and reward. In other words, dopamine systems are necessary for `wanting' incentives, but not for `liking' them or for learning new `likes' and `dislikes'.