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The cerebral cortex is critical for sensory processing and cognition, both of which are altered in autism spectrum disorders (ASDs). Cortical development relies on experience-dependent plasticity mechanisms, whose disruption has been suggested as a key biological mechanism of ASD. However, the effects of ASD-linked mutations on cortical development remain unknown. This project will address this knowledge gap by characterizing the consequences of mutations linked to ASDs on developing cortical circuitry in mouse models. To address the diverse genetics implicated in ASDs, this project will focus on two very different genetic mutations that present ASD-like symptoms in patients: CNTNAP2 and UBE3A. CNTNAP2 is widely implicated in ASDs via genome wide-association studies. UBE3A, when mutated in the maternal allele, produces several ASD symptoms and Angelman Syndrome. Recent reports have uncovered functional deficits in developing cortical circuitry to specific visual stimuli in specific higher visual cortical areas in both the CNTNAP2 and UBE3A models. This project will utilize 2-photon population calcium imaging to characterize the contributions of specific cell types to the observed differences in cortical activity. These results will reveal potential biological mechanisms of cortical dysfunction in ASDs, and provide detailed functional developmental profiles that can aid the development of therapies and biomarkers.