Autistic traits modulate frontostriatal connectivity during processing of rewarding faces

Sims, Thomas B.; Neufeld, Janina; Johnstone, Tom; Chakrabarti, Bhismadev

doi:10.1093/scan/nsu010

Cited by 28 publications

(39 citation statements)

References 63 publications

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“…A set of recent studies raises the possibility that some of these social behavioral deficits in ASD arise due to deficits in reward system functioning [73][74][75]. This hypothesis is supported by studies that report a lack of social motivation in children with autism [76,77].…”

Section: Autism and Reward Systemmentioning

confidence: 95%

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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Section: Autism and Reward Systemmentioning

confidence: 95%

Endocannabinoid Signaling in Autism

et al. 2015

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“…Nevertheless, attribution of specific OT effects to individual brain regions using functional magnetic resonance imaging of metabolic activity is complicated by recent evidence suggesting that OT stimulates the release of serotonin throughout the brain (49,123). (61,75,135,139,(142)(143)(144)150,153,155) Cognitive flexibility (144) Emotional empathy (217,232,336,337) Social recognition memory (162)(163)(164) ASD: hypersensitivity (301) Cognitive empathy (215,338,339) PTSD (340)(341)(342) ASD: dysmotivation (203,284,286,296) Anti social personality disorder (199,343) Extension of the organisational principle described above for parental, conjugal and consociate attachments to the regulation by OT of other affective, conative and cognitive functions (Table 1) is currently largely hypothetical, and awaits the future development of OT Cre lines specific for magnocellular and parvocellular cell types. Further characterisation of differential OT vesicular release mechanisms (124)(125)(126)(127)(128) will undoubtedly guide these efforts.…”

Section: Parallel Processingmentioning

confidence: 99%

Oxytocin: Parallel Processing in the Social Brain?

Dölen

2015

J Neuroendocrinology

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Early studies attempting to disentangle the network complexity of the brain exploited the accessibility of sensory receptive fields to reveal circuits made up of synapses connected both in series and in parallel. More recently, extension of this organisational principle beyond the sensory systems has been made possible by the advent of modern molecular, viral and optogenetic approaches. Here, evidence supporting parallel processing of social behaviours mediated by oxytocin is reviewed. Understanding oxytocinergic signalling from this perspective has significant implications for the design of oxytocin‐based therapeutic interventions aimed at disorders such as autism, where disrupted social function is a core clinical feature. Moreover, identification of opportunities for novel technology development will require a better appreciation of the complexity of the circuit‐level organisation of the social brain.

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“…First, the strength of conditioning was correlated to the number of ball tosses directed to the PosC face. Evaluative conditioning has already been seen to influence different proxy metrics related to empathy such as spontaneous mimicry of happy faces [Sims et al, ], or human hands [Haffey et al, ], cortical motor simulation [Trilla Gros, Panasiti, & Chakrabarti, ] and frontostriatal connectivity [Sims et al, ]. Importantly, evaluative conditioning is thought to contribute to several important phenomena in social psychology like stigmatization, and ingroup favoritism effect [Walther, Nagengast, & Trasselli, ] which respectively determine the way we categorize the social world and the way we favour some individuals (in‐group members) with respect to others (out‐group members).…”

Section: Discussionmentioning

confidence: 99%

“…All stimuli were selected from the standardized Mindreading set [Baron‐Cohen, Golan, Wheelwright, & Hill, 2004; available at http://www.jkp.com/mindreading]. These stimuli show sufficient inter‐rater reliability and external validity [Golan & Baron‐Cohen, ; Golan, Baron‐Cohen, & Hill, ], and have been used in previous research [Sims et al, ].…”

Section: Stimulus Materialsmentioning

confidence: 99%

“…In a similar experiment using evaluative conditioning of hand stimuli, individuals with high autistic traits were found to engage in less automatic mimicry for hands associated with high vs. low rewards [Haffey, Press, O'Connell, & Chakrabarti, ]. Finally, autistic traits have been shown to modulate the connectivity between ventral striatum an inferior frontal gyrus in response to high vs. low conditioned happy faces [Sims, Neufeld, Johnstone, & Chakrabarti, ]. To summarise, these studies have demonstrated how autistic traits modulate a connection between the reward value of social stimuli and the extent of spontaneous/automatic mimicry they elicit.…”

Section: Introductionmentioning

confidence: 99%

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Autistic Traits Moderate the Impact of Reward Learning on Social Behaviour

2015

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A deficit in empathy has been suggested to underlie social behavioural atypicalities in autism. A parallel theoretical account proposes that reduced social motivation (i.e., low responsivity to social rewards) can account for the said atypicalities. Recent evidence suggests that autistic traits modulate the link between reward and proxy metrics related to empathy. Using an evaluative conditioning paradigm to associate high and low rewards with faces, a previous study has shown that individuals high in autistic traits show reduced spontaneous facial mimicry of faces associated with high vs. low reward. This observation raises the possibility that autistic traits modulate the magnitude of evaluative conditioning. To test this, we investigated (a) if autistic traits could modulate the ability to implicitly associate a reward value to a social stimulus (reward learning/conditioning, using the Implicit Association Task, IAT); (b) if the learned association could modulate participants’ prosocial behaviour (i.e., social reciprocity, measured using the cyberball task); (c) if the strength of this modulation was influenced by autistic traits. In 43 neurotypical participants, we found that autistic traits moderated the relationship of social reward learning on prosocial behaviour but not reward learning itself. This evidence suggests that while autistic traits do not directly influence social reward learning, they modulate the relationship of social rewards with prosocial behaviour. Autism Res 2016, 9: 471–479. © 2015 The Authors Autism Research published by Wiley Periodicals, Inc. on behalf of International Society for Autism Research

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Autistic traits modulate frontostriatal connectivity during processing of rewarding faces

Cited by 28 publications

References 63 publications

Endocannabinoid Signaling in Autism

Endocannabinoid Signaling in Autism

Oxytocin: Parallel Processing in the Social Brain?

Autistic Traits Moderate the Impact of Reward Learning on Social Behaviour

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