Some autism spectrum disorders are caused by the improper expression of a gene termed UBE3A. Having duplications of the UBE3Agene is strongly associated with autism, while deletions of the UBE3A gene cause the severe intellectual disability “Angelman Syndrome”. Both disorders are characterized by cognitive, sensory, and behavioral deficits thought to arise because connections between brain neurons (synapses) form improperly during critical periods of development. However, little is known about how changes in UBE3A expression alter the wiring of neurons in the brain. This study aims to determine the role of UBE3A in the structural plasticity of synapses during critical periods of brain development. By filling this gap in knowledge, this study will not only reveal the synaptic structural dysfunction leading to improper circuit formation in UBE3A-related forms of autism, but may also serve as a model to help with therapeutic testing.