Orientation-specific surround suppression in the primary visual cortex varies as a function of autistic tendency

Flevaris, Anastasia V.; Murray, Scott O.

doi:10.3389/fnhum.2014.01017

Cited by 19 publications

(18 citation statements)

References 105 publications

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“…Another consideration when investigating differences between ASD and NT groups pertains to differences in neuropsychological data such as diagnosis severity or IQ ( Dinstein et al 2012 ; Brandwein et al 2015 ; Flevaris and Murray 2014 ). For example, Dinstein et al (2012 ) found a correlation of FSIQ and SNR of sensory response in ASD participants; they did not conduct the analyses on the NT participants.…”

Section: Discussionmentioning

confidence: 99%

An Examination of the Neural Unreliability Thesis of Autism

et al. 2016

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An emerging neuropathological theory of Autism, referred to here as “the neural unreliability thesis,” proposes greater variability in moment-to-moment cortical representation of environmental events, such that the system shows general instability in its impulse response function. Leading evidence for this thesis derives from functional neuroimaging, a methodology ill-suited for detailed assessment of sensory transmission dynamics occurring at the millisecond scale. Electrophysiological assessments of this thesis, however, are sparse and unconvincing. We conducted detailed examination of visual and somatosensory evoked activity using high-density electrical mapping in individuals with autism (N = 20) and precisely matched neurotypical controls (N = 20), recording large numbers of trials that allowed for exhaustive time-frequency analyses at the single-trial level. Measures of intertrial coherence and event-related spectral perturbation revealed no convincing evidence for an unreliability account of sensory responsivity in autism. Indeed, results point to robust, highly reproducible response functions marked for their exceedingly close correspondence to those in neurotypical controls

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Section: Discussionmentioning

confidence: 99%

An Examination of the Neural Unreliability Thesis of Autism

et al. 2016

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“…During passive language processing, negative BOLD responses were reduced in ASD, suggesting failure of inhibitory processes to induce regional deactivation(127). In controls, reduced orientation-specific surround suppression, reliant on lateral inhibition in visual receptive fields, associated with more autistic traits(128). Thus, task-based fMRI studies suggest neural disinhibition may associate with autism symptomatology in a continuous fashion, spanning into non-clinical populations.…”

Section: Functional Neuroimagingmentioning

confidence: 99%

Searching for Cross-Diagnostic Convergence: Neural Mechanisms Governing Excitation and Inhibition Balance in Schizophrenia and Autism Spectrum Disorders

Foss‐Feig

Adkinson

et al. 2017

Biological Psychiatry

247

183

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Recent theoretical accounts have proposed excitation (E) and inhibition (I) imbalance as a possible mechanistic, network-level hypothesis underlying neural and behavioral dysfunction across neurodevelopmental disorders, particularly autism spectrum disorder (ASD) and schizophrenia (SCZ). These two disorders share some overlap in their clinical presentation as well as convergence in their underlying genes and neurobiology. However, there are also clear points of dissociation in terms of phenotypes and putatively affected neural circuitry. Here we highlight emerging work from the clinical neuroscience literature examining neural correlates of E/I imbalance across children and adults with ASD and adults with both chronic and early-course SCZ. We discuss findings from diverse neuroimaging studies across distinct modalities, conducted with EEG, MEG, 1H-MRS, and fMRI, including effects observed both during task and at rest. Throughout this review we discuss points of convergence and divergence in the ASD and SCZ literature, with a focus on disruptions in neural E/I balance. We also consider these findings in relation to predictions generated by theoretical neuroscience, particularly computational models predicting E/I imbalance across disorders. Finally, we discuss how human non-invasive neuroimaging can benefit from pharmacological challenge studies to reveal mechanisms in ASD and SCZ. Collectively, we attempt to shed light on shared and divergent neuroimaging effects across disorders with the goal of informing future research examining the mechanisms underlying the E/I imbalance hypothesis across neurodevelopmental disorders. We posit that such translational efforts are vital to facilitate development of neurobiologically informed treatment strategies across neuropsychiatric conditions.

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“…3D), may be altered in autism (40,41). In one study, Foss-Feig et al (40) presented drifting gratings that varied in size and contrast, and had subjects indicate the direction of motion (left vs. right).…”

Section: Simulation 1: Visual Spatial Suppressionmentioning

confidence: 99%

A computational perspective on autism

Rosenberg

Patterson

Angelaki

2015

Proc. Natl. Acad. Sci. U.S.A.

149

151

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Autism is a neurodevelopmental disorder that manifests as a heterogeneous set of social, cognitive, motor, and perceptual symptoms. This system-wide pervasiveness suggests that, rather than narrowly impacting individual systems such as affection or vision, autism may broadly alter neural computation. Here, we propose that alterations in nonlinear, canonical computations occurring throughout the brain may underlie the behavioral characteristics of autism. One such computation, called divisive normalization, balances a neuron's net excitation with inhibition reflecting the overall activity of the neuronal population. Through neural network simulations, we investigate how alterations in divisive normalization may give rise to autism symptomatology. Our findings show that a reduction in the amount of inhibition that occurs through divisive normalization can account for perceptual consequences of autism, consistent with the hypothesis of an increased ratio of neural excitation to inhibition (E/I) in the disorder. These results thus establish a bridge between an E/I imbalance and behavioral data on autism that is currently absent. Interestingly, our findings implicate the context-dependent, neuronal milieu as a key factor in autism symptomatology, with autism reflecting a less "social" neuronal population. Through a broader discussion of perceptual data, we further examine how altered divisive normalization may contribute to a wide array of the disorder's behavioral consequences. These analyses show how a computational framework can provide insights into the neural basis of autism and facilitate the generation of falsifiable hypotheses. A computational perspective on autism may help resolve debates within the field and aid in identifying physiological pathways to target in the treatment of the disorder.A utism is a neurodevelopmental disorder that is dramatically increasing in prevalence (Fig. 1). Recent data place the number of children being diagnosed with autism in the United States at 1 in 68, more than doubling in the last decade (1-4). The disorder is highly pervasive, affecting individuals at cognitive, motor, and perceptual levels. It is furthermore a "spectrum disorder," with symptoms that manifest in varying degrees across individuals. This heterogeneity presents significant challenges to establishing a comprehensive characterization of the disorder.Research investigating the genetic and molecular basis of autism implicates over 100 genes (5), many of which are involved in synaptic development and function (6-8). As such, one prominent hypothesis is that autism arises from a neurophysiological excitation-to-inhibition (E/I) imbalance (9, 10). However, the connection between an E/I imbalance and the behavioral characteristics of the disorder remains unclear. Considering the pervasive nature of autism, and the covariance of loosely related symptoms (11-14), one possibility is that an E/I imbalance widely affects neural computation, in turn giving rise to the broad behavioral symptoms recognized as autism.Here,...

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Orientation-specific surround suppression in the primary visual cortex varies as a function of autistic tendency

Cited by 19 publications

References 105 publications

An Examination of the Neural Unreliability Thesis of Autism

An Examination of the Neural Unreliability Thesis of Autism

Searching for Cross-Diagnostic Convergence: Neural Mechanisms Governing Excitation and Inhibition Balance in Schizophrenia and Autism Spectrum Disorders

A computational perspective on autism

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