Individuals with autism spectrum disorder (ASD) often exhibit diverse abnormalities in somatosensory processing, including hypo- or hyper-sensitivity to tactile stimuli. Mutations in SHANK3, a gene encoding a synaptic scaffolding protein, have been repeatedly identified in ASD individuals. In this study, we employed aShank3mutant dog model to investigateASD-associated abnormalities in somatosensory processing. Compared with wild-type (WT) dogs, mutant animals exhibited reduced tactile sensitivity and tactile-evoked cortical responses in the somatosensory cortex. In addition, Shank3 mutant dogs showed decreased spectral powers of resting-state brain oscillations at all frequencies. Given the efficacy of the γ-aminobutyric acid A receptor (GABA_AR) antagonist pentylenetetrazole (PTZ) in enhancing resting-state brain oscillations, we tried PTZ as a potential intervention. PTZ ameliorated the abnormalities in both tactile reactivity and brain oscillations, and also improved dog-human social interactions in Shank3 mutant dogs. Our findings underscore a pivotal role of Shank3 in somatosensory processing and suggest GABA_AR antagonists as prospective therapeutic agents for a subset of ASD patients.