While the precise causes of autism is not yet known, multiple genetic and environmental factors are thought to play an important impact on the development of the disorder. The site where certain neurons connect, called gap junctions, are sensitive to environmental agents and have downstream effects on cell growth and reproduction, and possibly on migration of neuronal precursors to their appropriate destinations. In order to manipulate the function of the gap junction in an animal model, the investigators will test the effects of an NSAID which alters the function of gap junctions on the activity of neurons during development and migration. Deficits in neuronal migration and formation of different layers of the cortex may lead to the neuropathological and behavioral features observed by other scientists. The mentor and the fellow will use advanced molecular biology techniques to trace the position of the migrated neurons during critical periods of neuronal development. They will also study properties of the misplaced neurons to determine their abilities to participate in a functional network. Finally, behavioral analysis of offspring exposed to prenatal NSAIDS will be performed. This will help better link any neurobiological differences with functional outcomes, especially as they relate to the symptoms of autism spectrum disorder. What this means for people with autism: Using disruption of the gap junction by biophysical and environmental factors will help identify the cause of cortical malformation. This will be relevant to a better understanding of brain development as well as the causes of autism spectrum disorders.