![]() ![]() All participants reported no history of neurological disorder and had normal or corrected-to-normal vision. ![]() ASD classification was based on DSM-5 diagnostic criteria and confirmed using the Autism Diagnostic Observation Schedule, Second Edition (ADOS-2) (Lord et al., 2012). Seven high-functioning medication-free children with ASD and seven neurotypical (NT) children from 6 – 14 years of age were recruited (ASD M: 9.89, SD: 2.31 NT M: 9.89, SD: 2.90). To validate this paradigm, we demonstrated that healthy adults have delayed processing in conditions of large/high-contrast thought to reflect surround suppression (p=0.013) as indexed by N1 ERP latency. To our knowledge, there have been no prior studies to investigate an ERP marker of surround suppression. ![]() a selective enhancement of motion perception in conditions of large, high-contrast stimuli (Foss-Feig et al., 2013 Horder et al., 2014). Behaviorally, individuals with ASD have demonstrated weakened surround suppression, i.e. Behavioral studies have demonstrated that healthy adults have a directional impairment of discrimination in conditions of large/high-contrast visual stimuli, which is thought to reflect surround suppression of motion selective neurons and to be driven by GABA (Tadin et al., 2003 Aaen-Stockdale et al., 2009). To explore possible consequences of imbalanced GABA:Glu neurotransmission on the visual system, we investigated surround suppression in ASD using a visual motion processing task during electroencephalography (EEG) recording to derive the N1 event related potential (ERP). Emergent evidence suggests that hyper- or hypo-reactivity to sensory input(s) in ASD may be due to a neurochemical imbalance between excitatory glutamate (Glu) and inhibitory γ-aminobutyric acid (GABA) neurotransmission, also known as the excitatory:inhibitory (E:I) theory of ASD. Sensory processing abnormalities are a core feature of Autism Spectrum Disorder (ASD). ![]()
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