Sensory integration difficulties have been reported in autism, but their underlying braincircuit mechanisms are underexplored. Using five autism-related mouse models, Shank3+/ΔC, Mecp2 R308/Y , Cntnap2−/−, L7-Tsc1 (L7/Pcp2 Cre ::Tsc1 flox/+ ), and patDp(15q11-13)/+, we report specific perturbations in delay eyeblink conditioning, a form of associative sensory learning requiring cerebellar plasticity. By distinguishing perturbations in the probability and characteristics of learned responses, we

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... found that probability was reduced in Cntnap2−/−, patDp(15q11-13)/+, and L7/Pcp2 Cre ::Tsc1 flox/+ , which are associated with Purkinje-cell/deep-nuclear gene expression, along with Shank3+/ΔC. Amplitudes were smaller in L7/Pcp2 Cre ::Tsc1 flox/+ as well as Shank3+/ΔC and Mecp2 R308/Y , which are associated with granule cell pathway expression. Shank3+/ΔC and Mecp2 R308/Y also showed aberrant response timing and reduced Purkinje-cell dendritic spine density. Overall, our observations are potentially accounted for by defects in instructed learning in the olivocerebellar loop and response representation in the granule cell pathway. Our findings indicate that defects in associative temporal binding of sensory events are widespread in autism mouse models.