Evidence map›Paper›PMID 17072591›Full record

ReviewPsychopharmacology2007

The debate over dopamine's role in reward: the case for incentive salience.

Kent C Berridge

Registry-linked trialAbstract readReview
PubMed Publisher
In one paragraph

Review in Psychopharmacology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03068793 (Multimodal Neural Investigation of Reward Processing in Mental Illness), which is not on this map. Cited by 989 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
989citing papers in PubMed, 4 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

NCT03068793 completednot on this mapstarted 2013, after this paper: background citation

Multimodal Neural Investigation of Reward Processing in Mental Illness

TypeobservationalSponsorSusanna FryerRan2013 to 2019Enrolled80ConditionsEarly-onset SchizophreniaArmsElectroencephalography (EEG) and Magnetic Resonance Imaging (MRI)
3 · Its place in the literature

Who cites it

989 citing papers in PubMed, 4 syntheses or guidelines pooled it.

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  14. Music engages the phasic dopaminergic D1-receptor system in humans: a PET-fMRI study using [European journal of nuclear medicine and molecular imaging · 2026
    Article
  15. Identifying behavioral and biological predictors of cannabis vapor self-administration in rats.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
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  19. Addiction biology · 2026
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929 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author.

Kent C BerridgeDepartment of Psychology, University of Michigan, 530 Church Street (East Hall), Ann Arbor, MI 48109, USA. berridge@umich.edu

Funding

Affective neuroscience of taste reactivityR01MH063649 · NIMH · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI BERRIDGE, KENT C. · 2002 to 2024
$7.8M
Cue-triggered Reward SeekingR01DA015188 · NIDA · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI BERRIDGE, KENT C. · 2003 to 2021
$4.9M
Neural Coding of Reward in Ventral ForebrainR01DA017752 · NIDA · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ALDRIDGE, J WAYNE · 2005 to 2009
$1.5M
NIDA NIH HHS DA015188NIDA NIH HHS DA017752NIMH NIH HHS MH63649
6 · The paper itself

Abstract

introductionDebate continues over the precise causal contribution made by mesolimbic dopamine systems to reward. There are three competing explanatory categories: 'liking', learning, and 'wanting'. 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'. In brief, recent evidence indicates that dopamine is neither necessary nor sufficient to mediate changes in hedonic 'liking' for sensory pleasures. 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. By contrast, growing evidence indicates that dopamine does contribute causally to incentive salience. Dopamine appears necessary for normal 'wanting', and dopamine activation can be sufficient to enhance cue-triggered incentive salience. Drugs of abuse that promote dopamine signals short circuit and sensitize dynamic mesolimbic mechanisms that evolved to attribute incentive salience to rewards. Such drugs interact with incentive salience integrations of Pavlovian associative information with physiological state signals. That interaction sets the stage to cause compulsive 'wanting' in addiction, but also provides opportunities for experiments to disentangle 'wanting', 'liking', and learning hypotheses. Results from studies that exploited those opportunities are described here.

conclusionIn short, dopamine's contribution appears to be chiefly to cause 'wanting' for hedonic rewards, more than 'liking' or learning for those rewards.

Indexed as

MotivationRewardAnimalsAppetitive BehaviorAssociation LearningBehavior, AddictiveDopamineHumansLimbic SystemNeurotransmitter AgentsNucleus AccumbensProsencephalonReinforcement, PsychologyDopamineNeurotransmitter Agents

Identifiers

What OpenQuestion holds

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Registered trials

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.