Audiovisual processing is selectively impaired in the primary visual cortex but not in the posterior parietal cortex of a mouse model of Fragile X syndrome

Abstract

Sensory processing disruptions are a common feature in various forms of autism spectrum disorders (ASD), yet the circuit-level mechanisms underlying these deficits remain poorly understood. Here, we examined differences in audiovisual processing between wild-type and Fmr1-knockout (KO) mice, a model of Fragile X syndrome, which itself represents the most common hereditary cause of autism. We performed multi-area Neuropixels probe recordings in the primary visual cortex (V1) and posterior parietal cortex (PPC) of head-fixed, anesthetized mice being shown visual and auditory stimuli. Previous studies generally reported sensory hypersensitivity in Fragile X mice. In contrast, we observed reduced visual and auditory responses in V1 (but not PPC) of Fragile X compared to wild-type mice. Auditory stimuli reduced the amplitude of visual responses in both V1 and PPC across the two lines, but a dependency on the relative timing of the two sensory modalities was only observed in wild-type mice. Our results provide evidence for a region-specific sensory-processing phenotype of ASD, something that needs to be taken into account when evaluating the efficacy of pharmacological and behavioral strategies to address ASD symptoms.