Abstract:According to the social motivation theory of autism, children who develop Autism Spectrum Disorder (ASD) have early deficits in social motivation, which is expressed by decreased attention to social information. These deficits are said to lead to impaired socio-cognitive development, such as theory of mind (ToM). There is little research focused on the relation between social motivation and ToM in this population. The goal of the present study was to investigate the link between one aspect of social motivation… Show more
“…FBR positive effects on social behavior could be related to the modulation of mesolimbic dopaminergic transmission [5,32], as blunted NAcS dopaminergic response to a natural reward is an index of motivational anhedonia and the rescued response is accompanied by restored motivation to operate for the reward [5,15,42]. Overall, these results support the hypothesis that social motivational deficits contribute to the impaired social behavior [3,8]. Hence, a rationale is suggested for early pharmacological interventions that facilitate motivational mechanisms targeting core social symptoms in male and female subjects.…”
Section: Discussionsupporting
confidence: 66%
“…This study aimed at challenging the social motivational theory of ASD that interprets the core social deficit of the disorder as an impairment of social rewardprocessing mechanisms that drive sociality [3,4,8]. In mammals, the dopaminergic projections from VTA to Fig.…”
Section: Discussionmentioning
confidence: 99%
“…Here, utilizing the validated environmental model of ASD induced by prenatal exposure to valproic acid (VPA) [7], we report the behavioral and neurochemical effects of FBR administered to rats from weaning (postnatal day 21, PND 21) to young adulthood (PND [48][49][50][51][52][53]. We focused on the developmental window between weaning and late adolescence since ASD children show early deficits in social motivation that during development lead to sociocognitive deficits [3,8], and adolescence is the critical period for the development of high-order cognitive functions [9]. The prevalence of ASD diagnosis in male subjects suggests sex-related phenotypic differences in the clinical presentation [10].…”
Background: The social motivational theory of autism spectrum disorder (ASD) focuses on social anhedonia as key causal feature of the impaired peer relationships that characterize ASD patients. ASD prevalence is higher in boys, but increasing evidence suggests underdiagnosis and undertreatment in girls. We showed that stress-induced motivational anhedonia is relieved by repeated treatment with fenofibrate (FBR), a peroxisome proliferator-activated receptor α (PPARα) agonist. Here, we used the valproic acid (VPA) model of ASD in rats to examine male and female phenotypes and assess whether FBR administration from weaning to young adulthood relieved social impairments. Methods: Male and female rats exposed to saline or VPA at gestational day 12.5 received standard or FBR-enriched diet from postnatal day 21 to 48-53, when behavioral tests and ex vivo neurochemical analyses were performed. Phosphorylation levels of DARPP-32 in response to social and nonsocial cues, as index of dopamine D 1 receptor activation, levels of expression of PPARα, vesicular glutamatergic and GABAergic transporters, and postsynaptic density protein PSD-95 were analyzed by immunoblotting in selected brain regions. Results: FBR administration relieved social impairment and perseverative behavior in VPA-exposed male and female rats, but it was only effective on female stereotypies. Dopamine D 1 receptor signaling triggered by social interaction in the nucleus accumbens shell was blunted in VPA-exposed rats, and it was rescued by FBR treatment only in males. VPA-exposed rats of both sexes exhibited an increased ratio of striatal excitatory over inhibitory synaptic markers that was normalized by FBR treatment. Limitations: This study did not directly address the extent of motivational deficit in VPA-exposed rats and whether FBR administration restored the likely decreased motivation to operate for social reward. Future studies using operant behavior protocols will address this relevant issue.
“…FBR positive effects on social behavior could be related to the modulation of mesolimbic dopaminergic transmission [5,32], as blunted NAcS dopaminergic response to a natural reward is an index of motivational anhedonia and the rescued response is accompanied by restored motivation to operate for the reward [5,15,42]. Overall, these results support the hypothesis that social motivational deficits contribute to the impaired social behavior [3,8]. Hence, a rationale is suggested for early pharmacological interventions that facilitate motivational mechanisms targeting core social symptoms in male and female subjects.…”
Section: Discussionsupporting
confidence: 66%
“…This study aimed at challenging the social motivational theory of ASD that interprets the core social deficit of the disorder as an impairment of social rewardprocessing mechanisms that drive sociality [3,4,8]. In mammals, the dopaminergic projections from VTA to Fig.…”
Section: Discussionmentioning
confidence: 99%
“…Here, utilizing the validated environmental model of ASD induced by prenatal exposure to valproic acid (VPA) [7], we report the behavioral and neurochemical effects of FBR administered to rats from weaning (postnatal day 21, PND 21) to young adulthood (PND [48][49][50][51][52][53]. We focused on the developmental window between weaning and late adolescence since ASD children show early deficits in social motivation that during development lead to sociocognitive deficits [3,8], and adolescence is the critical period for the development of high-order cognitive functions [9]. The prevalence of ASD diagnosis in male subjects suggests sex-related phenotypic differences in the clinical presentation [10].…”
Background: The social motivational theory of autism spectrum disorder (ASD) focuses on social anhedonia as key causal feature of the impaired peer relationships that characterize ASD patients. ASD prevalence is higher in boys, but increasing evidence suggests underdiagnosis and undertreatment in girls. We showed that stress-induced motivational anhedonia is relieved by repeated treatment with fenofibrate (FBR), a peroxisome proliferator-activated receptor α (PPARα) agonist. Here, we used the valproic acid (VPA) model of ASD in rats to examine male and female phenotypes and assess whether FBR administration from weaning to young adulthood relieved social impairments. Methods: Male and female rats exposed to saline or VPA at gestational day 12.5 received standard or FBR-enriched diet from postnatal day 21 to 48-53, when behavioral tests and ex vivo neurochemical analyses were performed. Phosphorylation levels of DARPP-32 in response to social and nonsocial cues, as index of dopamine D 1 receptor activation, levels of expression of PPARα, vesicular glutamatergic and GABAergic transporters, and postsynaptic density protein PSD-95 were analyzed by immunoblotting in selected brain regions. Results: FBR administration relieved social impairment and perseverative behavior in VPA-exposed male and female rats, but it was only effective on female stereotypies. Dopamine D 1 receptor signaling triggered by social interaction in the nucleus accumbens shell was blunted in VPA-exposed rats, and it was rescued by FBR treatment only in males. VPA-exposed rats of both sexes exhibited an increased ratio of striatal excitatory over inhibitory synaptic markers that was normalized by FBR treatment. Limitations: This study did not directly address the extent of motivational deficit in VPA-exposed rats and whether FBR administration restored the likely decreased motivation to operate for social reward. Future studies using operant behavior protocols will address this relevant issue.
“…Autism is characterized by deficits in social interaction, communication, and behavioral flexibility. Cognitive functioning in persons with autism, related to behavioral symptomatology, has been reported largely within the domains of theory of mind [14], executive functioning [15] and central [16]. So, there are several core underlying capabilities/deficits that coexist in ASD and that contribute to the pathogenesis of autism [17].…”
Background: Over the past ten years, the authors have been designing, developing, and testing pervasive technology to support children with autism (ASD). Methods: In the present study, an integrated system based on multimedia and augmented interaction technologies have been tested on young subjects with ASD and dyspraxia in the age range of 6–10 years, in charge for rehabilitation treatments; a team of clinical psychologists has analyzed the results of the experimentation. The ten children involved in the project underwent an initial assessment of praxis skills and motor coordination. Subsequently, the subjects were subdivided into two subgroups: five children participated in the experimentation and five were evaluated as the control group (treatment as usual). Results: The evaluation showed an increased score in the several aspects considered, and particularly those related to motor coordination. An improvement in balancing tests and in hands-movement testing was found. Conclusion: The children involved in the sessions showed greater ability to self-control the movement as well as to select specific motor areas. The methods used seem to be promising to improve emotional and social skills too in a motivating and enjoyable climate. A high level of acceptance by professionals was observed and parents’ feedback was also positive.
“…ASD is a classic example. Although the problems that people with ASD have with figurative language have been explained in terms of either a cognitive deficit affecting the Theory of Mind (Happé, 1995 ), or a language deficit per se , particularly, in semantic competence (Norbury, 2004 ), we cannot ignore that mastering both abilities needs a rich social environment (see Syal and Finlay, 2011 ; Burnside et al, 2017 , and references therein). Following our line of evidence, our hypothesis is that these disparate deficits (problems with figurative language, with non-figurative language, and with socialization) result from the impairment of a common underlying biological mechanism that was remodeled during our recent evolutionary history.…”
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