Degraded tactile coding in the Cntnap2 mouse model of autism.

ABSTRACT: Atypical sensory processing in autism involves altered neural circuit function and neural coding in sensory cortex, but the nature of coding disruption is poorly understood. We characterized neural coding in L2/3 of whisker somatosensory cortex (S1) of Cntnap2^-/- mice, an autism model with pronounced hypofunction of parvalbumin (PV) inhibitory circuits. We tested for both excess spiking, which is often hypothesized in autism models with reduced inhibition, and alterations in somatotopic coding, using c-fos immunostaining and 2-photon calcium imaging in awake mice. In Cntnap2^-/- mice, c-fos-(+) neuron density was elevated in L2/3 of S1 under spontaneous activity conditions, but comparable to control mice after whisker stimulation, suggesting that sensory-

SUBMITTER: Wang HC 

PROVIDER: S-EPMC10557772 | biostudies-literature | 2023 Sep

REPOSITORIES: biostudies-literature