The DOI matches its Crossref record; 353 of the 353 references it cites were found in a registry or an index.
The neural basis of drug craving: An incentive-sensitization theory of addiction
Abstract
This paper presents a biopsychological theory of drug addiction, the 'Incentive-Sensitization Theory'. The theory addresses three fundamental questions. The first is: why do addicts crave drugs? That is, what is the psychological and neurobiological basis of drug craving? The second is: why does drug craving persist even after long periods of abstinence? The third is whether 'wanting' drugs (drug craving) is attributable to 'liking' drugs (to the subjective pleasurable effects of drugs)? The theory posits the following. (1) Addictive drugs share the ability to enhance mesotelencephalic dopamine neurotransmission. (2) One psychological function of this neural system is to attribute 'incentive salience' to the perception and mental representation of events associated with activation of the system. Incentive salience is a psychological process that transforms the perception of stimuli, imbuing them with salience, making them attractive, 'wanted', incentive stimuli. (3) In some individuals the repeated use of addictive drugs produces incremental neuroadaptations in this neural system, rendering it increasingly and perhaps permanently, hypersensitive ('sensitized') to drugs and drug-associated stimuli. The sensitization of dopamine systems is gated by associative learning, which causes excessive incentive salience to be attributed to the act of drug taking and to stimuli associated with drug taking. It is specifically the sensitization of incentive salience, therefore, that transforms ordinary 'wanting' into excessive drug craving. (4) It is further proposed that sensitization of the neural systems responsible for incentive salience ('for wanting') can occur independently of changes in neural systems that mediate the subjective pleasurable effects of drugs (drug 'liking') and of neural systems that mediate withdrawal. Thus, sensitization of incentive salience can produce addictive behavior (compulsive drug seeking and drug taking) even if the expectation of drug pleasure or the aversive properties of withdrawal are diminished and even in the face of strong disincentives, including the loss of reputation, job, home and family. We review evidence for this view of addiction and discuss its implications for understanding the psychology and neurobiology of addiction.
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In the citing paper
“The incentive sensitization theory has afforded valuable insight into the neurobiological and behavioral processes that are associated with individual vulnerability to addictive spectrum pathology, such as substance use disorders (T. E. Robinson & Berridge, 1993) and more recently, gambling disorder (Linnet, 2014; M. J. F. Robinson, Fischer, Ahuja, Lesser, & Maniates, 2015b; Rømer Thomsen et al.,”
From Cued for Risk: Evidence for an Incentive Sensitization Framework to Explain the Interplay between Stress and Anxiety, Substance Abuse, and Reward Uncertainty in Disordered Gambling Behavior (2019) · cites this paper as T. E. Robinson & Berridge, 1993
In the citing paper
“This system is comprised of dopaminergic fibers that project from the ventral tegmental area in the midbrain, to limbic and cortical structures such as the nucleus accumbens, ventral pallidum, amygdala, and prefrontal cortex (Di Chiara & Imperato, 1988; T. E. Robinson & Berridge, 1993).”
From Cued for Risk: Evidence for an Incentive Sensitization Framework to Explain the Interplay between Stress and Anxiety, Substance Abuse, and Reward Uncertainty in Disordered Gambling Behavior (2019) · cites this paper as T. E. Robinson & Berridge, 1993
In the citing paper
“Often referred to as incentive salience, it is the psychological process by which rewards and the cues associated with them become imbued with subconscious motivational value and are transformed into objects of desire (M. J. F. Robinson, Robinson, & Berridge, 2013; T. E. Robinson & Berridge, 1993; 2008).”
From Cued for Risk: Evidence for an Incentive Sensitization Framework to Explain the Interplay between Stress and Anxiety, Substance Abuse, and Reward Uncertainty in Disordered Gambling Behavior (2019) · cites this paper as T. E. Robinson & Berridge, 1993
In the citing paper
“The incentive sensitization theory (T. E. Robinson & Berridge, 1993; 2008) was initially proposed to distinguish between the different components of reward.”
From Cued for Risk: Evidence for an Incentive Sensitization Framework to Explain the Interplay between Stress and Anxiety, Substance Abuse, and Reward Uncertainty in Disordered Gambling Behavior (2019) · cites this paper as T. E. Robinson & Berridge, 1993
In the citing paper
“The incentive-sensitization theory of addiction(16, 17) also emphasizes sensitization process, but specifies that repeated use of a drug produces neuroadapations that sensitize motivational reward to drugs and associated drug stimuli (i.e.., processes of “wanting”) distinct from the neurocircuitry mediating hedonic reward (liking) which may not sensitize over time.”
From A Prospective 5-Year Re-examination of Alcohol Response in Heavy Drinkers Progressing in Alcohol Use Disorder (2016) · cites this paper as [16]
In the citing paper
“which may not sensitize over time.”
From A Prospective 5-Year Re-examination of Alcohol Response in Heavy Drinkers Progressing in Alcohol Use Disorder (2016) · cites this paper as [16]
In the citing paper
“Significant methodological differences across studies, i.e., sample size, subject characteristics, alcohol dose, route of administration, and degree of naturalism to usual contexts(16, 83), hamper direct comparisons to discern the source of this discrepancy.”
From A Prospective 5-Year Re-examination of Alcohol Response in Heavy Drinkers Progressing in Alcohol Use Disorder (2016) · cites this paper as [16]
In the citing paper
“The attribution of incentive salience is the product of previous experience (i.e., learned associations) interacting with an individual’s genetic propensity and neurobiological state 16,24–27.”
From A selective role for dopamine in stimulus-reward learning (2011) · cites this paper as [25]
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Metadata
- Authors
- Robinson, T.
- Affiliations
- University of Michigan (US)
- Corresponding author
- Robinson, T
- Venue
- Brain Research Reviews
- Publisher
- Elsevier BV
- Published
- 1993-12
- Volume
- 18
- Issue
- 3
- Pages
- 247-291
- ISSN
- 0165-0173 (ISSN-L)
- OpenAlex
- W2106862702
- Semantic Scholar
- 2993069cd29bb6b2cf86cba46b145119d2095bc9
- Cited by
- 7,346
- References
- 353
- Citations by year
- 2026: 173 · 2025: 199 · 2024: 165 · 2023: 222 · 2022: 239 · 2021: 245 · 2020: 327 · 2019: 318 · 2018: 239 · 2017: 264 · 2016: 286 · 2015: 306 · 2014: 324 · 2013: 325 · 2012: 302
- FWCI
- 25.06
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Brain Research Reviews (publishedVersion)
- PubMed (publishedVersion)
- Deep Blue (University of Michigan) (submittedVersion)
- Funders
- National Institutes of Health (5r01ns023959-06)
- U.S. Public Health Service
- National Institute on Drug Abuse
- National Institute of Neurological Disorders and Stroke (NS-23959)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Health Sciences › Medicine › Epidemiology › Substance Abuse Treatment and Outcomes
- Life Sciences › Neuroscience › Cognitive Neuroscience › Neural and Behavioral Psychology Studies
- Keywords
- drug craving, incentive-sensitization theory, drug addiction, incentive salience, dopamine signaling, sensitization, neural adaptation, associative learning, drug-seeking behavior, drug liking, withdrawal, compulsive drug taking, abstinence
- MeSH terms
- Adaptation, Physiological, Animals, Brain, Conditioning, Psychological, Corpus Striatum, Dopamine, Humans, Models, Neurological, Motivation, Nucleus Accumbens, Recurrence, Reinforcement, Psychology, Substance-Related Disorders
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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