![]() We hypothesized that the ASD group would be characterized by decreased striatal phasic DA release in response to incentives relative to a control group, indexed by the nondisplaceable binding potential (BP ND) of raclopride. ![]() ![]() Neutral and rewarding incentives were presented during a behavioral fMRI task, and a bolus+infusion raclopride PET paradigm allowed measurement of both dopaminergic tone and phasic dopaminergic release in response to incentives. The goal of this study was to use simultaneous fMRI and positron emission tomography (PET) with the D2/D3 dopamine receptor antagonist raclopride to investigate striatal functioning during incentive processing in ASD. ĭespite converging evidence supporting the involvement of striatal DA impairments in the pathophysiology of ASD, no molecular imaging study has investigated striatal DA functioning in ASD. Finally, a widely used ASD preclinical model, the valproic acid model, causes a cascade of neurobiological changes including excitatory/inhibitory neural imbalances linked to increased basal DA in the frontal cortex, hyperactive mesocortical DA in response to stress, and changes in locomotor behavior akin to that observed in striatal DA-depleted animals. Of note, there are dense oxytocin projections within the mesolimbic DA system, including oxytocin neurons that project to the ventral tegmental area and nucleus accumbens, and oxytocin receptor activation plays an important role in the activation of reward pathways during prosocial behaviors. Furthermore, oxytocin abnormalities in ASD, reports of the therapeutic effects of intranasal oxytocin administration for treating core ASD symptoms, and the effects of oxytocin on striatal responses to rewards in ASD support an etiologically-relevant role for mesolimbic DA functioning in ASD. Second, polymorphisms of the DA D4 receptor gene and the DA transporter gene are related to challenging behaviors and repetitive behaviors in ASD, and there are links between polymorphisms of the DA-3-receptor gene and striatal volumes and repetitive behaviors in ASD. First, there is evidence of impaired striatal functioning in ASD in the form of altered effort-based decision-making for rewards. Additional findings indicate that striatal DA dysfunction is implicated in the etiology of ASD. Numerous functional magnetic resonance imaging (fMRI) studies have reported that ASD is characterized by decreased striatal responses to rewards, highlighting striatal involvement in impaired social motivation in ASD. This DA system mediates responses to social and nonsocial incentives, and striatal DA transmission influences social behaviors. Social motivation is supported by the same substrates that govern other motivated behaviors, namely ascending dopamine (DA) projections from the ventral tegmental area to the striatum and prefrontal cortex, forming a DA pathway sensitive to reward magnitude and probability. ![]() ![]() When children with ASD lack the motivation to participate in activities where social skills are typically forged, the resulting impoverished social environment compounds social impairments and negatively impacts the development of social communication. In particular, this framework posits that social communication symptoms in autism spectrum disorder (ASD) reflect decreased motivation to engage in reciprocal social behaviors throughout development that results in fewer experiences with social rewards. The social motivation hypothesis of autism proposes that functional disruptions in brain circuits supporting social motivation constitute a primary deficit that contributes to social communication impairments. ![]()
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