Summary: I find that the AS mouse model has impaired communication and motor behavior during early postnatal development, enhanced seizure-like activity and an abnormal cortical electroencephalogram (EEG). Reducing the levels of ARC reversed the enhanced seizure-like activity and EEG, but not the communication or motor deficits. The specific rescue of seizure-like activity by reducing ARC, but not EPHEXIN5, reveals a role for molecular diversity in the development of behavioral circuits. Further, these findings suggest that therapeutic interventions that reduce the level of ARC expression have the potential to reverse the seizures associated with AS. Lastly, the identification of aberrant behaviors in AS mice provides clues regarding the neural circuit defects that occur in AS and ultimately allow new approaches for treating this disorder, and broader ASDs.