Abstract
Increased neural excitation resulting from weakened inhibition is a leading hypothesis for the pathophysiology of autism. However, experimental support in humans remains equivocal. Alternatively, modulatory processes that suppress neural responses but do not specifically rely on inhibition may be impacted in ASD. Leveraging well-characterized suppressive neural circuits in the visual system, we used behavioral and fMRI tasks to demonstrate a significant reduction in neural suppression in young adults with ASD compared to neurotypical controls. We further tested the mechanism of this suppression by measuring levels of the inhibitory neurotransmitter GABA, and found no differences in GABA between groups. We show how a computational model that incorporates divisive normalization, as well as narrower top-down gain (that could result, for example, from a narrower window of attention), can explain our observations and divergent previous findings. Thus, weaker neural suppression in ASD may be attributable to differences in top-down processing, but not to differences in GABA levels.
