Autism Spectrum Disorder (ASD) is characterized by impairments in social communication and interactions, as well as restricted behaviours. Strikingly most of ASD patients also exhibit aberrant reactivity to sensory stimuli including tactile stimuli. Tactile information is perceived in the periphery and processed in the spinal cord under the control of inhibitory neurons before being sent to higher brain structures. However, whether these inhibitory neurons undergo functional alterations in ASD models remains poorly investigated. To explore the functional plasticity of those neurons in ASD, we used Fmr1-/y mice crossed with GAD67-GFP reporter lines to visualize spinal GABAergic neurons (SGN) and characterized their electrophysiologic, transcriptomic and morphologic properties in acute spinal slices using the patch-seq technique. We demonstrate that Fmr1-/y-GAD67-GFP mice display tactile deficits (longer latencies in tape removal test, decreased reactivity to brush stimulation), but also decreased anxiety in elevated plus maze, and lowered social scores in the nest building test. Second, we show that SGN display lowered excitability (decreased spike firing frequency for highest current injections, and increased medium after-hyperpolarisation amplitude to repetitive current stimulations). Third, we show SGN in Fmr1-/y display less complex dendritic arborization especially in islet cells. Finally, we demonstrate that SGN in Fmr1-/y and wild-type littermates exhibit different transcriptomic profiles, highlighting an interesting regulation of some high-risk ASD genes. Altogether, we suggest that functional alterations of SGN in ASD models contributes to abnormal tactile information processing upstream to the brain and may play an important role in the development of sensory and social deficits characterizing ASD.