Abnormalities in brain structures and sleep disturbances are extensive in many neurological disorders, including autism.  In the present study, we used 16p11.2df mice that possess a deletion on chromosome 7 syntenic with a region on human chromosome 16 (the 16p11.2 region). In humans, deletions and duplications in this chromosomal region are associated with autism, thereby studying the deletion in a rodent model may be useful in discovering novel prognosticators for autism.  Previous research has shown that adult 16p11.2/del mice display motor deficits and differences in sleep-wake behavior.  Importantly, both motor and sleep-wake dysfunction have also been observed in individuals with autism.  In the first study, we looked at sleep-wake cyclicity in week-old 16p11.2df mice by recording muscle activity as animals cycled normally between sleep and wake.  In a second study, we assessed the cerebellar structure of wildtype and 16p11.2df at 2 weeks of age.  If we observe differences in sleep-wake patterning between wildtype and 16p11.2/del mice, we can infer that these sleep-wake cyclicity differences are the result of changes in neural pathways involved in behavioral state expressed in autism.  Furthermore, if cerebellar structure is different in wildtype and 16p11.2df mice it may provide one mechanism by which motor behavior is affected in adulthood.  In sum, both studies aim to determine whether behavioral and neuroanatomical differences found in this model can be observed during the early postnatal period. By improving our ability to predict risk for autism early in life, we may, through early intervention, improve outcomes.