Reward Circuitry Function in Autism During Face Anticipation and Outcomes

Dichter, Gabriel S.; Richey, J. Anthony; Rittenberg, Alison; Sabatino, Antoinette; Bodfish, James W.

doi:10.1007/s10803-011-1221-1

Cited by 201 publications

(215 citation statements)

References 116 publications

(130 reference statements)

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“…This finding is consistent with previous research examining the effect of reward type on task performance, which indicates that children with ASD may be less motivated by social than non-social rewards [480,565-568]. Dichter and colleagues [569] recently reported results of an fMRI study of reward anticipation and outcome using monetary and social (faces) rewards within the context of an incentive-delay task. The ASD group displayed bilateral amygdala hyperactivation during face-reward anticipation and bilateral insular cortex hyperactivation during face-reward outcomes.…”

Section: Reviewsupporting

confidence: 89%

Reward circuitry dysfunction in psychiatric and neurodevelopmental disorders and genetic syndromes: animal models and clinical findings

Dichter

Damiano

Allen

2012

J Neurodevelop Disord

245

207

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This review summarizes evidence of dysregulated reward circuitry function in a range of neurodevelopmental and psychiatric disorders and genetic syndromes. First, the contribution of identifying a core mechanistic process across disparate disorders to disease classification is discussed, followed by a review of the neurobiology of reward circuitry. We next consider preclinical animal models and clinical evidence of reward-pathway dysfunction in a range of disorders, including psychiatric disorders (i.e., substance-use disorders, affective disorders, eating disorders, and obsessive compulsive disorders), neurodevelopmental disorders (i.e., schizophrenia, attention-deficit/hyperactivity disorder, autism spectrum disorders, Tourette’s syndrome, conduct disorder/oppositional defiant disorder), and genetic syndromes (i.e., Fragile X syndrome, Prader–Willi syndrome, Williams syndrome, Angelman syndrome, and Rett syndrome). We also provide brief overviews of effective psychopharmacologic agents that have an effect on the dopamine system in these disorders. This review concludes with methodological considerations for future research designed to more clearly probe reward-circuitry dysfunction, with the ultimate goal of improved intervention strategies.

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Section: Reviewsupporting

confidence: 89%

Reward circuitry dysfunction in psychiatric and neurodevelopmental disorders and genetic syndromes: animal models and clinical findings

Dichter

Damiano

Allen

2012

J Neurodevelop Disord

245

207

View full text Add to dashboard Cite

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“…Arbib and Mundhenk (2005) extended this proposal and suggested that dysfunctions in the mirror neuron system may also contribute to deficits in self-monitoring in schizophrenia. Pathological conditions that express deficits in social cognition and social functioning have also been found to have underlying abnormalities in reward processing, including ASDs (Dichter, Richey, Rittenberg, Sabatino, & Bodfish, 2012;Scott-Van Zeeland, Dapretto, Ghahremani, Poldrack, & Bookheimer, 2010) and schizophrenia (Gold, Waltz, Prentice, Morris, & Heerey, 2008). It may be the case that in such clinical populations, patients may have abnormal experiences of reward and punishment from social stimuli, caused by an underlying general breakdown in reward processing.…”

Section: Discussionmentioning

confidence: 99%

Modulation of motor cortex activity when observing rewarding and punishing actions

et al. 2013

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a b s t r a c tInterpreting others' actions is essential for understanding the intentions and goals in social interactions. Activity in the motor cortex is evoked when we see another person performing actions, which can also be influenced by the intentions and context of the observed action. No study has directly explored the influence of reward and punishment on motor cortex activity when observing others' actions, which is likely to have substantial relevance in different social contexts. In this experiment, EEG was recorded while participants watched movie clips of a person performing actions that led to a monetary reward, loss or no change for the observer. Using the EEG mu rhythm as an index of motor resonance, our results demonstrate that observation of rewarding actions produce significantly greater motor cortex activity than punishing or neutral actions, with punishing actions producing greater activity than neutral ones. In addition, the dynamic change in the mu rhythm over sensorimotor cortex is modulated by reward and punishment, with punishing actions producing a prolonged suppression. These findings demonstrate that the associated reward value of an observed action may be crucial in determining the strength of the representation of the action in the observer's brain. Consequently, reward and punishment is likely to drive observational learning through changes in the action observation network, and may also influence how we interpret, understand, engage in and empathize with others' actions in social interaction.

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“…An early study using a continuous performance task found no behavioral evidence for group differences in trials with monetary rewards versus nonrewards [78]. Similarly, comparable behavioral performance in a reward-processing task using a variant of the go-no-go task was found in children and adults with and without ASD [79,80]. In contrast, using a similar task, DeMurie et al [81] demonstrated that children with ASD were slower in responding to social rewards than monetary rewards, but this was not specific to ASD.…”

Section: Autism and Reward Systemmentioning

confidence: 98%

Endocannabinoid Signaling in Autism

et al. 2015

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Autism spectrum disorder (ASD) is a complex behavioral condition with onset during early childhood and a lifelong course in the vast majority of cases. To date, no behavioral, genetic, brain imaging, or electrophysiological test can specifically validate a clinical diagnosis of ASD. However, these medical procedures are often implemented in order to screen for syndromic forms of the disorder (i.e., autism comorbid with known medical conditions). In the last 25 years a good deal of information has been accumulated on the main components of the Bendocannabinoid (eCB) system^, a rather complex ensemble of lipid signals (Bendocannabinoids^), their target receptors, purported transporters, and metabolic enzymes. It has been clearly documented that eCB signaling plays a key role in many human health and disease conditions of the central nervous system, thus opening the avenue to the therapeutic exploitation of eCB-oriented drugs for the treatment of psychiatric, neurodegenerative, and neuroinflammatory disorders. Here we present a modern view of the eCB system, and alterations of its main components in human patients and animal models relevant to ASD. This review will thus provide a critical perspective necessary to explore the potential exploitation of distinct elements of eCB system as targets of innovative therapeutics against ASD.Key Words Autism spectrum disorder . endocannabinoid system . fragile X syndrome . metabolic regulation . reward system The Endocannabinoid SystemTwenty-five years after the cloning and expression of a complementary DNA that encoded a G protein-coupled receptor, named type-1 cannabinoid (CB 1 ) receptor [1], there is a good deal of information on the main components of the so-called Bendocannabinoid (eCB) system^, as well as on its role in controlling cannabinergic signaling in human health and disease [2][3][4]. Anandamide (AEA) and 2-arachidonoylglycerol (2-AG) are the most active eCBs as yet identified, although this family of bioactive lipids includes other arachidonic acid (AA) derivatives with cannabimimetic properties (i.e., noladin ether, virodhamine, N-arachidonoyldopamine, to name but a few). The classical dogma that eCBs are synthesized and released Bon demand^upon (patho)physiological stimuli has been recently revisited on the basis of unexpected evidence for intracellular reservoirs and transporters of eCBs. These new entities have been shown to drive intracellular trafficking of eCBs, adding a new dimension to the regulation of their biological activity [5]. To date, several metabolic routes have B. Chakrabarti, A. Persico and N. Battista are equal first authors.

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Reward Circuitry Function in Autism During Face Anticipation and Outcomes

Cited by 201 publications

References 116 publications

Reward circuitry dysfunction in psychiatric and neurodevelopmental disorders and genetic syndromes: animal models and clinical findings

Reward circuitry dysfunction in psychiatric and neurodevelopmental disorders and genetic syndromes: animal models and clinical findings

Modulation of motor cortex activity when observing rewarding and punishing actions

Endocannabinoid Signaling in Autism

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