Cited by 197Autism Spectrum Disorder ResearchNeuroendocrine regulation and behaviorNeurotransmitter Receptor Influence on Behavior

The DOI matches its Crossref record; 239 of the 239 references it cites were found in a registry or an index; 10 of the 182 sources its claims cite were checked for support.

Social “wanting” dysfunction in autism: neurobiological underpinnings and treatment implications

Open access
Kohls, Gregor, Chevallier, Coralie, Troiani, Vanessa, Schultz, Robert T·2012·Journal of Neurodevelopmental Disorders

Abstract

Most behavioral training regimens in autism spectrum disorders (ASD) rely on reward-based reinforcement strategies. Although proven to significantly increase both cognitive and social outcomes and successfully reduce aberrant behaviors, this approach fails to benefit a substantial number of affected individuals. Given the enormous amount of clinical and financial resources devoted to behavioral interventions, there is a surprisingly large gap in our knowledge of the basic reward mechanisms of learning in ASD. Understanding the mechanisms for reward responsiveness and reinforcement-based learning is urgently needed to better inform modifications that might improve current treatments. The fundamental goal of this review is to present a fine-grained literature analysis of reward function in ASD with reference to a validated neurobiological model of reward: the 'wanting'/'liking' framework. Despite some inconsistencies within the available literature, the evaluation across three converging sets of neurobiological data (neuroimaging, electrophysiological recordings, and neurochemical measures) reveals good evidence for disrupted reward-seeking tendencies in ASD, particularly in social contexts. This is most likely caused by dysfunction of the dopaminergic-oxytocinergic 'wanting' circuitry, including the ventral striatum, amygdala, and ventromedial prefrontal cortex. Such a conclusion is consistent with predictions derived from diagnostic criteria concerning the core social phenotype of ASD, which emphasize difficulties with spontaneous self-initiated seeking of social encounters (that is, social motivation). Existing studies suggest that social 'wanting' tendencies vary considerably between individuals with ASD, and that the degree of social motivation is both malleable and predictive of intervention response. Although the topic of reward responsiveness in ASD is very new, with much research still needed, the current data clearly point towards problems with incentive-based motivation and learning, with clear and important implications for treatment. Given the reliance of behavioral interventions on reinforcement-based learning principles, we believe that a systematic focus on the integrity of the reward system in ASD promises to yield many important clues, both to the underlying mechanisms causing ASD and to enhancing the efficacy of existing and new interventions.

Overview

AI snapshot

Written from the paper’s full text.

TL;DR

This review applies the Berridge ‘wanting’/‘liking’ framework to autism spectrum disorder (ASD) and concludes that social reward ‘wanting’ is disrupted, most likely via dopaminergic–oxytocinergic circuitry including the ventral striatum, amygdala, and ventromedial prefrontal cortex, whereas evidence for compromised ‘liking’ is inconclusive. It argues that social motivation varies among individuals with ASD, is malleable, and predicts intervention response, with implications for reinforcement-based treatments.

Key findings

  • Across three converging neurobiological data sets (fMRI, electrophysiology, neurochemistry), the review finds good evidence for disrupted reward-seeking tendencies in ASD, particularly in social contexts; this is attributed to dysfunction of dopaminergic–oxytocinergic ‘wanting’ circuitry (ventral striatum, amygdala, ventromedial prefrontal cortex).
  • Four out of five published fMRI studies reported diminished ventral striatum activation in ASD compared with typically developing controls when processing social or monetary reward versus non-reward; vmPFC (‘liking’) findings were mixed, with two studies reporting stronger and two reporting lower activation in ASD for monetary reward.
  • ERP evidence from only three reports suggested outcome-related responses (e.g., FRN/P3 to monetary gain/loss) were relatively intact in ASD, whereas anticipatory responses (e.g., cue-related P3, SPN) were atypical, especially for social reward.
  • The paper states that the percentage of affected children who profit from behavioral treatment, let alone reach optimal outcome, ranges from 3% to 50%, and that stronger social approach/‘wanting’ at treatment onset predicts better response to early intensive behavioral interventions.

Methods

  • Design: narrative literature review using the validated ‘wanting’/‘liking’ neurobiological model of reward as an analytic framework.
  • Data: published functional neuroimaging, electrophysiological (ERP/EEG), and neurochemical/neuropeptide studies of reward responsiveness in ASD, with emphasis on social versus non-social reward.
  • Analysis: qualitative synthesis evaluating whether findings support predicted disruptions in ‘wanting’ (ventral striatum, dopamine, anticipatory ERPs) versus ‘liking’ (vmPFC, opioids, outcome ERPs); no meta-analysis or systematic search strategy is reported.

Limitations

  • The paper states that the ASD reward literature is very new, with few studies and inconsistent findings, making firm conclusions premature; it also notes methodological shortcomings such as lack of research on biological rewards, neglected physiological/drive states, and low ecological validity of many reward stimuli.
  • The paper states that phenotypic heterogeneity, comorbid traits (e.g., depression, anxiety, inattention/hyperactivity), sleep deficits, and temperament/intrinsic motivation differences can affect reward sensitivity and treatment response, and that laboratory-based measures quantifying reward responsiveness in ASD are lacking.
  • Evident from the text: as a narrative review, it does not report a systematic search strategy, formal risk-of-bias assessment, or quantitative synthesis, so the conclusions rest on a small and methodologically varied set of studies.

Model-written summary. Check it against the paper before relying on it.

Integrity signals

Registry

Crossref · 10.1186/1866-1955-4-10

Cites

239 of 239 references verified0 citation errors · 0 not checkable

Statistics

Nothing to recompute.

Figures

Figure 1 A simplified view of the time course of reward processing and its underlying neural correlates (after Berridge and Kringelbach[[7]]). Temporally, the processing of reward can be subdivided into two successive phases, with a ‘wanting’ period usually preceding a ‘liking’ response, each with a discrete neural basis. Although rewards that are ‘liked’ are typically also ‘wanted’, it seems that these two aspects of reward are dissociable both psychologically and neurobiologically. Rewarding situations are characterized by an anticipation phase or the ‘wanting’ of a reward, which often results in a phase of reward consumption or ‘liking’, with some rewards causing a peak level of subjective pleasantness (for example, a lottery win, job promotion, encounter with an old friend, favorite meal or music, sexual orgasm, drug high). Many rewarding episodes are followed by a period of satiation for the specific reward experienced. To our knowledge, there are currently no data available to suggest that the ‘wanting’/’liking’ model would apply differently to social and non-social types of reward. However, some rewards lack satiation effects or result in only short periods of satiation (for example, money). In general, physiological or drive states (for example, satiation, deprivation, stress, anxiety) strongly modulate an individual’s responsiveness to reward. Both reward ‘wanting’ and reward ‘liking’ have been associated with discrete (and to a specific extent with some overlapping) neural correlates. Whereas ‘wanting’ is mainly driven by phasic dopaminergic neural firing in the ventral striatum (including the nucleus accumbens), ‘liking’ is largely influenced by the opioid system, and recruits the ventromedial prefrontal cortex (vmPFC). As summarized in this paper, there is good evidence to suggest that reward ‘wanting’ is disrupted in ASD, particularly in the social domain, whereas the available data for reward ‘liking’ are inconclusive (see below for details).
Figure 1 A simplified view of the time course of reward processing and its underlying neural correlates (after Berridge and Kringelbach[[7]]). Temporally, the processing of reward can be subdivided into two successive phases, with a ‘wanting’ period usually preceding a ‘liking’ response, each with a discrete neural basis. Although rewards that are ‘liked’ are typically also ‘wanted’, it seems that these two aspects of reward are dissociable both psychologically and neurobiologically. Rewarding situations are characterized by an anticipation phase or the ‘wanting’ of a reward, which often results in a phase of reward consumption or ‘liking’, with some rewards causing a peak level of subjective pleasantness (for example, a lottery win, job promotion, encounter with an old friend, favorite meal or music, sexual orgasm, drug high). Many rewarding episodes are followed by a period of satiation for the specific reward experienced. To our knowledge, there are currently no data available to suggest that the ‘wanting’/’liking’ model would apply differently to social and non-social types of reward. However, some rewards lack satiation effects or result in only short periods of satiation (for example, money). In general, physiological or drive states (for example, satiation, deprivation, stress, anxiety) strongly modulate an individual’s responsiveness to reward. Both reward ‘wanting’ and reward ‘liking’ have been associated with discrete (and to a specific extent with some overlapping) neural correlates. Whereas ‘wanting’ is mainly driven by phasic dopaminergic neural firing in the ventral striatum (including the nucleus accumbens), ‘liking’ is largely influenced by the opioid system, and recruits the ventromedial prefrontal cortex (vmPFC). As summarized in this paper, there is good evidence to suggest that reward ‘wanting’ is disrupted in ASD, particularly in the social domain, whereas the available data for reward ‘liking’ are inconclusive (see below for details).CC BY · PubMed Central
Figure 2 The neural circuitry of reward ‘wanting’ versus reward ‘liking’. The neural circuitry of reward ‘wanting’ comprises the ventral striatum (VS; blue), while that for reward ‘liking’ comprises the ventromedial prefrontal cortex, including the orbitofrontal cortex (OFC) and the dorsal and ventral anterior cingulate cortex (dACC, vACC) (green), which closely interacts with the amygdala (AMY = orange) and the midbrain, including the ventral tegmental area (VTA; purple). This complex network interfaces with motor-related areas and other higher cognitive associative cortices (not shown here) to translate basic reward information into appropriate goal-directed action plans to achieve a desired reward.
Figure 2 The neural circuitry of reward ‘wanting’ versus reward ‘liking’. The neural circuitry of reward ‘wanting’ comprises the ventral striatum (VS; blue), while that for reward ‘liking’ comprises the ventromedial prefrontal cortex, including the orbitofrontal cortex (OFC) and the dorsal and ventral anterior cingulate cortex (dACC, vACC) (green), which closely interacts with the amygdala (AMY = orange) and the midbrain, including the ventral tegmental area (VTA; purple). This complex network interfaces with motor-related areas and other higher cognitive associative cortices (not shown here) to translate basic reward information into appropriate goal-directed action plans to achieve a desired reward.CC BY · PubMed Central

Verification

Claims the paper makes

96 Not checked yet · 34 Own interpretation · 4 Partly supported · 2 Supported · 1 No basis given · accuracy not yet measured

Verify all 172 references — free account

Show all 84 claims

  • It may state two separate claims as one. 49
  • Probably not a substantial claim. 8
53 of 53
  • The paper relies on this without support.

    Most behavioral training regimens in ASD rely on reward-based reinforcement strategies.

    “Most behavioral training regimens in autism spectrum disorders (ASD) rely on reward-based reinforcement strategies.”
  • The paper relies on this without support.

    There is a surprisingly large gap in knowledge concerning basic reward mechanisms in ASD.

    “Given the enormous amount of clinical and financial resources devoted to behavioral interventions, there is a surprisingly large gap in our knowledge of the basic reward mechanisms of learning in ASD.”
  • The paper relies on this without support.

    Current ASD research lacks a clear reference to any validated neurobiological model of reward.

    “Because current ASD research lacks a clear reference to any validated neurobiological model of reward, we introduce a well-established framework of reward responsiveness formulated by Berridge and colleagues: the ‘wanting’/’liking’ model [7,8].”
  • The paper relies on this without support.

    There are currently no data available to suggest that the ‘wanting’/’liking’ model would apply differently to social and non-social types of reward.

    “To our knowledge, there are currently no data available to suggest that the ‘wanting’/’liking’ model would apply differently to social and non-social types of reward.”
  • The paper relies on this without support.

    To date, little is known about reward function in ASD, and conflicting evidence comes from intervention programs versus experimental research.

    “To date, little is known about reward function in ASD, and conflicting evidence comes from intervention programs versus experimental research.”
  • The paper relies on this without support.

    The paradoxical finding of efficacious treatments rooted in reinforcement strategies in combination with weaker reward systems in ASD has received little attention.

    “To date, the paradoxical finding of efficacious treatments rooted in reinforcement strategies in combination with weaker reward systems in ASD has received little attention in the field.”
  • The paper relies on this without support.

    Current experimental and intervention research in ASD tends to construe reward as a unitary phenomenon, lacking a clear reference to any validated neurobiological model.

    “In particular, a potentially important limitation of current experimental and intervention research in ASD is that it tends to construe reward as a unitary phenomenon, lacking a clear reference to any validated neurobiological model of reward; however, a critical examination of reward function in ASD requires a more fine-grained analytic approach.”
  • The paper relies on this without support.

    There are currently no objective behavioral markers of ‘liking’ and ‘wanting’, so it is necessary to draw on neurobiological measures.

    “Given that there are currently no objective behavioral markers of ‘liking’ and ‘wanting’, it is necessary to draw on neurobiological measures.”
  • The paper relies on this without support.

    It is not yet understood how and why behavioral approaches work well for some people with ASD but not for others.

    “It is not yet understood how and why behavioral approaches work well for some people with ASD but not for others.”
  • The authors state this as an assumption.

    The social motivation impairment in ASD is attributable, at least partially, to dysfunction of the dopaminergic–oxytocinergic vmPFC–VS–amygdala brain network.

    “The theory assumes that the social motivation impairment is attributable, at least partially, to dysfunction of the dopaminergic–oxytocinergic vmPFC–VS–amygdala brain network [2,40].”
10 of 10

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

Each contradiction between two passages listed here was confirmed by an independent check.

2 of 2

Citations

Cites

Cited by

Sorted by citations

See all 197

Metadata

Authors
Kohls, G., Chevallier, C., Troiani, V., & Schultz, R. T.
Affiliations
Children's Hospital of Philadelphia (US)
Corresponding author
Kohls, Gregor
Venue
Journal of Neurodevelopmental Disorders
Published
2012-06-27
Volume
4
Issue
1
Pages
10-10
ISSN
  • 1866-1947 (ISSN-L)
  • 1866-1955
OpenAlex
W2164121118
Cited by
197
References
239
Citations by year
2026: 4 · 2025: 14 · 2024: 11 · 2023: 14 · 2022: 11 · 2021: 17 · 2020: 18 · 2019: 19 · 2018: 14 · 2017: 10 · 2016: 15 · 2015: 20 · 2014: 19 · 2013: 9 · 2012: 2
FWCI
8.20
Type
journal article
Language
en
Open access
Locations
  • Journal of Neurodevelopmental Disorders (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
Funders
  • National Science Foundation
  • Robert Wood Johnson Foundation (66727)
  • Pennsylvania Department of Health (4100042728, 4100047863)
  • National Institute of Mental Health (R01-MH073084)
Topics
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Autism Spectrum Disorder Research
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Neuroendocrine regulation and behavior
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
Keywords
autism spectrum disorder, reward processing, social motivation, ventral striatum, amygdala, ventromedial prefrontal cortex, behavioral interventions, individual differences in treatment response

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.

A language model drew the claims from the paper on 2026-10-10, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).

A second model labelled each claim on 2026-10-10 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).

Cited sources are checked with a language model’s help (gpt-6-sol).

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 ›

Are you an author, or do you see a problem with this page? Request a review