Atypical sensory development is found in both human patients and SHANK3 knockout mice. It is known that genes associated with ASD (in this case SHANK3) can shape and affect cerebellum circuit functions, and that changes in the cerebellum affect behavior and cognition. Because of this knowledge, effectiveness of the cerebellum at responding to sensory input and general function of the cerebellum were measured in this study, in addition to the prevalence of ASD symptoms. A method of sensory conditioning was used to study the effect of cerebellar associative sensory learning defects in SHANK3 knockout mice. The SHANK3 knockout mice had delayed or absent responses to stimuli following sensory conditioning, indicating defects in the cerebellum. This suggests that SHANK3, which is typically heavily concentrated in the cerebellum, is partially responsible for regulating sensory learning.
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