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Cited by 580Neurotransmitter Receptor Influence on BehaviorNeural and Behavioral Psychology StudiesSchizophrenia research and treatment

Dopamine and reward: The anhedonia hypothesis 30 years on

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Wise, Roy A.·2008·Neurotoxicity Research
DOI 10.1007/bf03033808PMC PMC3155128
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Abstract

The anhedonia hypothesis--that brain dopamine plays a critical role in the subjective pleasure associated with positive rewards--was intended to draw the attention of psychiatrists to the growing evidence that dopamine plays a critical role in the objective reinforcement and incentive motivation associated with food and water, brain stimulation reward, and psychomotor stimulant and opiate reward. The hypothesis called to attention the apparent paradox that neuroleptics, drugs used to treat a condition involving anhedonia (schizophrenia), attenuated in laboratory animals the positive reinforcement that we normally associate with pleasure. The hypothesis held only brief interest for psychiatrists, who pointed out that the animal studies reflected acute actions of neuroleptics whereas the treatment of schizophrenia appears to result from neuroadaptations to chronic neuroleptic administration, and that it is the positive symptoms of schizophrenia that neuroleptics alleviate, rather than the negative symptoms that include anhedonia. Perhaps for these reasons, the hypothesis has had minimal impact in the psychiatric literature. Despite its limited heuristic value for the understanding of schizophrenia, however, the anhedonia hypothesis has had major impact on biological theories of reinforcement, motivation, and addiction. Brain dopamine plays a very important role in reinforcement of response habits, conditioned preferences, and synaptic plasticity in cellular models of learning and memory. The notion that dopamine plays a dominant role in reinforcement is fundamental to the psychomotor stimulant theory of addiction, to most neuroadaptation theories of addiction, and to current theories of conditioned reinforcement and reward prediction. Properly understood, it is also fundamental to recent theories of incentive motivation.

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  • Every drug with addictive potential increases dopamine in the nucleus accumbens, through either activation/disinhibition of dopaminergic neurons in the ventral tegmental area or activation of synaptic mechanisms that lead to increased dopamine concentration at the terminals of these neurons in the nucleus accumbens.

    “Specifically, every drug with addictive potential increases dopamine in the nucleus accum bens, through either activation/disinhibition of dopaminergic neurons in the ventral tegmental area or activation of synaptic mechanisms that lead to increased dopamine concentration at the terminals of these neurons in the nucleus accumbens 34 .”

    From Substance use disorders: a comprehensive update of classification, epidemiology, neurobiology, clinical aspects, treatment and prevention (2023) · cites this paper as [34]

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  • The mesoaccumbens dopamine pathway mediates rewarding properties of reinforcers, including modulation of motivation.

    “The mesoaccumbens dopamine pathway mediates a variety of rewarding properties of reinforcers including the modulation of motivation (Schultz, 2006; Wise, 2008).”

    From Imaging addiction: D2 receptors and dopamine signaling in the striatum as biomarkers for impulsivity (2014) · cites this paper as Wise, 2008

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Research works printed but not linked: 3

  1. Carlsson A Costa E Garattini S Amphetamine and brain catecholamines Amphetamines and Related Compounds 1970 New York Raven Press 289 300
  2. Stein L Efron DH Chemistry of reward and punishment Proceedings of the American College of NeuroPsychophar-macology 1968 Washington, DC U.S. Government Printing Office 105 123
  3. Wise CD Stein L Costa E Garattini S Amphetamine: facilitation of behavior by augmented release of norepinephrine from the medial forebrain bundle Amphetamines and Related Compounds 1970 New York Raven Press 463 485

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Authors
Wise, R. A.
Affiliations
National Institutes of Health (US)
Corresponding author
Wise, Roy A.
ORCID
Wise, Roy A.
Venue
Neurotoxicity Research
Publisher
Springer Science and Business Media LLC
Published
2008-06
Volume
14
Issue
2-3
Pages
169-183
ISSN
  • 1029-8428 (ISSN-L)
  • 1476-3524
DOI
10.1007/bf03033808
PMC
PMC3155128
OpenAlex
W1994609215
Cited by
580
References
150
Citations by year
2026: 5 · 2025: 20 · 2024: 20 · 2023: 27 · 2022: 22 · 2021: 31 · 2020: 73 · 2019: 34 · 2018: 32 · 2017: 30 · 2016: 36 · 2015: 42 · 2014: 38 · 2013: 36 · 2012: 42
FWCI
13.27
Type
journal article
Language
en
Open access
Licence
www.springer.com/tdm (tdm)
Locations
  • Neurotoxicity Research (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institutes of Health
  • National Institute on Drug Abuse (ZIADA000471)
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Neural and Behavioral Psychology Studies
  • Health Sciences › Medicine › Psychiatry and Mental health › Schizophrenia research and treatment
Keywords
dopamine, reward, reinforcement, incentive motivation, schizophrenia, antipsychotic drugs, psychostimulants, opiates, brain stimulation reward, addiction, conditioned reinforcement, reward prediction, synaptic plasticity, learning and memory
MeSH terms
Animals, Dopamine, Humans, Models, Psychological, Motivation, Nucleus Accumbens, Philosophy, Reinforcement, Psychology, Reward, Schizophrenia, Antipsychotic Agents, Behavior, Addictive, Rats

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