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Abstract
One recent, promising account of Autism Spectrum Disorders (ASD) situates the cause of the disorder in an atypicality in basic neural information processing, more specifically in how activity of one neuron is modulated by neighboring neurons. The canonical neural computation that implements such contextual influence is called divisive (or suppressive) normalization. The account proposes that this normalization is reduced in ASD. We tested one fundamental prediction of this model for low-level perception, namely that individuals with ASD would show reduced cross-orientation suppression (leading to an illusory tilt perception). 11 young adults with an ASD diagnosis and 12 age-, gender-, and IQ-matched control participants performed a psychophysical orientation perception task with compound grating stimuli. Illusory tilt perception did not differ significantly between groups, indicating typical divisive normalization in individuals with ASD. In fact, all individuals with ASD showed a considerable orientation bias. There was also no correlation between illusory tilt perception and autistic traits as measured by the Social Responsiveness Scale. These results provide clear evidence against the decreased divisive normalization model of ASD in low-level perception, where divisive normalization is best characterized. We evaluate the broader existing evidence for this model and propose ways to salvage and refine the model.
Highlights
In recent years several neurocomputational theories of Autism Spectrum Disorders (ASD) appeared
Contrary to the Divisive normalization (DN) account of ASD, we found no reduced cross-orientation suppression in participants with ASD compared to matched control participants
All participants with ASD showed a level of illusory tilt perception that was comparable to or even stronger than that of typical participants
Summary
In recent years several neurocomputational theories of Autism Spectrum Disorders (ASD) appeared. In contrast to the traditional neurocognitive accounts of ASD, these models enable more specific, model-based predictions of differences in perceptual or cognitive performance between people with and without ASD1–3 One such model is derived from a neural population coding model on divisive normalization in the early visual cortex[3]. The denominator of the equation consists of a semi-saturation constant c50 which determines the horizontal shift in the response function (see Fig. 1), and the divisive normalization signal, which reflects the linear response of an inhibitory gain control pool of neurons. The orientation tuning function of the gain control pool, g, is identical to f, except that the orientation bandwidth of g is typically much broader Due to this normalization signal, the response of a neuron i to a stimulus with a particular contrast and orientation is inhibited by the responses of neurons in the suppressive pool which respond to a much broader range of orientations. For stimuli of small size and contrast, the difference in performance between ASD and controls disappeared, consistent with negligible spatial suppression in this condition (little power in the denominator c, little impact of differing κ’s)
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