Cited by 218Neurotransmitter Receptor Influence on BehaviorNeural and Behavioral Psychology StudiesGambling Behavior and Treatments

“Liking” and “Wanting” Linked to Reward Deficiency Syndrome (RDS): Hypothesizing Differential Responsivity in Brain Reward Circuitry

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Blum, Kenneth, Gardner, Eliot, Oscar-Berman, Marlene, Gold, Mark·2012·Current Pharmaceutical Design

Abstract

In an attempt to resolve controversy regarding the causal contributions of mesolimbic dopamine (DA) systems to reward, we evaluate the three main competing explanatory categories: "liking,""learning," and "wanting" [1]. That is, DA may mediate (a) the hedonic impact of reward (liking), (b) learned predictions about rewarding effects (learning), or (c) the pursuit of rewards by attributing incentive salience to reward-related stimuli (wanting). We evaluate these hypotheses, especially as they relate to the Reward Deficiency Syndrome (RDS), and we find that the incentive salience or "wanting" hypothesis of DA function is supported by a majority of the evidence. Neuroimaging studies have shown that drugs of abuse, palatable foods, and anticipated behaviors such as sex and gaming affect brain regions involving reward circuitry, and may not be unidirectional. Drugs of abuse enhance DA signaling and sensitize mesolimbic mechanisms that evolved to attribute incentive salience to rewards. Addictive drugs have in common that they are voluntarily selfadministered, they enhance (directly or indirectly) dopaminergic synaptic function in the nucleus accumbens (NAC), and they stimulate the functioning of brain reward circuitry (producing the "high" that drug users seek). Although originally believed simply to encode the set point of hedonic tone, these circuits now are believed to be functionally more complex, also encoding attention, reward expectancy, disconfirmation of reward expectancy, and incentive motivation. Elevated stress levels, together with polymorphisms of dopaminergic genes and other neurotransmitter genetic variants, may have a cumulative effect on vulnerability to addiction. The RDS model of etiology holds very well for a variety of chemical and behavioral addictions.

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Authors
Blum, K., Gardner, E., Oscar-Berman, M., & Gold, M.
Affiliations
  • University of Florida (US)
  • National Institute on Drug Abuse (US)
Venue
Current Pharmaceutical Design
Published
2012-01-01
Volume
18
Issue
1
Pages
113-118
ISSN
1381-6128 (ISSN-L)
OpenAlex
W2127079332
Cited by
218
References
56
Citations by year
2026: 9 · 2025: 7 · 2024: 10 · 2023: 7 · 2022: 11 · 2021: 8 · 2020: 51 · 2019: 11 · 2018: 7 · 2017: 12 · 2016: 13 · 2015: 19 · 2014: 25 · 2013: 18 · 2012: 9
FWCI
9.36
Type
journal article
Language
en
Open access
Locations
  • Current Pharmaceutical Design (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
National Institute on Alcohol Abuse and Alcoholism (R01 AA07112, K05AA00219, R01AA007112, K05AA000219)
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Neural and Behavioral Psychology Studies
  • Social Sciences › Psychology › Clinical Psychology › Gambling Behavior and Treatments
Keywords
reward deficiency syndrome, incentive salience, wanting, liking, mesolimbic dopamine system, brain reward system, nucleus accumbens, addiction, self-administration, reward expectancy, stress, behavioral addiction, chemical dependence
MeSH terms
Animals, Brain, Dopamine, Humans, Reward, Syndrome, Signal Transduction, Behavior, Addictive, Substance-Related Disorders, Neuroimaging

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