Degraded tactile coding in the Cntnap2 mouse model of autism.

Atypical sensory processing is common in autism, but how neural coding is disrupted in sensory cortex is unclear. We evaluate whisker touch coding in L2/3 of somatosensory cortex (S1) in Cntnap2 ^−/− mice, which have reduced inhibition. This classically predicts excess pyramidal cell spiking, but this remains controversial, and other deficits may dominate. We find that c-fos expression is elevated in S1 of Cntnap2 ^−/− mice under spontaneous activity conditions but is comparable to that of control mice after whisker stimulation, suggesting normal sensory-evoked spike rates. GCaMP8m imaging from L2/3 pyramidal cells shows no excess whisker responsiveness, but it does show multiple signs of degraded somatotopic coding. This includes broadened whisker-tuning curves, a blurred whisker map, and blunted whisker point representations. These disruptions are greater in noisy than in sparse sensory conditions. Tuning instability across days is also substantially elevated in Cntnap2 ^−/− . Thus, Cntnap2 ^−/− mice show no excess sensory-evoked activity, but a degraded and unstable tactile code in S1. [Display omitted] • Characterizes sensory coding in S1 cortex in the Cntnap2 ^−/− mouse model of autism • Broad tuning and blurred, unstable maps, but no excess sensory-evoked spiking • Reduced inhibition is associated with degraded, unstable sensory coding in Cntnap2 ^−/− mice Wang and Feldman characterize tactile coding abnormalities in whisker S1 cortex in the Cntnap2 ^−/− mouse model of autism. These mice show multiple signs of degraded sensory coding, including blurred maps and unstable tuning, but not excess spiking. Impaired discriminative coding may be a common feature of the sensory cortex in autism. [ABSTRACT FROM AUTHOR]