Altered sensory experience is one of the core features of autism, affecting approximately 90% of autistic individuals, exerting a strong negative influence on day-to-day life and contributing to the development of other core symptoms and medical conditions that co-occur with autism. Touch is particularly crucial during development and tactile alterations in autistic individuals include differences in stimulus perception and sensory-related neural excitability. Better understanding and synthetizing these features is crucial in characterizing altered tactile experience in autism and can provide insight into the development of other core features. In this study, we characterized tactile alterations in Fmr1-/y mice, a genetic mouse model of autism. To study perception at the behavioral and neuronal level, we developed a novel vibrotactile perceptual decision-making task that can be combined with measurements of neuronal activity and translated in human studies. Our findings recapitulate the tactile alterations observed in autistic individuals, with task acquisition deficits, higher detection thresholds leading to perceptual hyposensitivity, and increased inter-individual and intra-individual variability in the Fmr1-/y mice. Parallel in vivo calcium imaging recordings of neuronal activity of excitatory and inhibitory neurons in the primary somatosensory cortex revealed that a decreased signal-to-noise ratio phenotype in the Fmr1-/y mice underlies perceptual alterations. To examine whether these alterations are malleable to pharmacological treatment, we targeted the voltage- and calcium-sensitive K+ channel BKCa, an approach previously shown to correct cellular hyperexcitability. Altogether, our results expand our knowledge of tactile alterations in autism and suggest objective biomarkers that can be used for developing mechanism-based treatment.