Diminished signal-to-noise ratio disrupts somatosensory population encoding and drives tactile hyposensitivity in the Fmr1-/y autism model.

Abstract

Touch is essential for interacting with the world, and atypical tactile experience is a core feature of autism that profoundly affects daily life. However, we do not know the neural mechanisms of low-level tactile perception and their alterations in autism. Using a translational perceptual task, we recapitulate the multifaceted tactile features of autistic individuals in the Fmr1-/y mouse model of autism, showing tactile hyposensitivity, interindividual variability, and unreliable responses. We reveal that impaired detection decoding in Fmr1-/y-hyposensitive mice stems from diminished single-neuron signal-to-noise ratio in the primary somatosensory cortex that leads to weak population encoding of the tactile stimulus and its detection. This manifests as reduced stimulus-dependent neural recruitment, impaired response precision, and disrupted ensemble dynamics. Decreasing neuronal hyperexcitability strengthens sensory encoding and improves tactile perception. This work provides a translational framework for probing neuronal-perceptual changes in neurodevelopmental conditions, reveals inter-individual variability in preclinical models, and uncovers the neural basis of tactile hyposensitivity in autism.