Our lab's research is utilizing multiple rodent models of autism to examine the neurobiology of the disorder. In addition to examining social interactions, and repetitive behavior, the lab will be examining changes in cognitive flexibility and multisensory processing. We are using the VPA (valproic acid) model of autism because it has both construct and face validity and provides a way to examine behavioral changes developmentally. The second model is a model of Fragile X syndrome, which is the number one cause of intellectual disability. Fragile X rats are created by modifying the Fmr1 gene (Fmr1 knock out) which results in the loss of FMR protein. Projects include looking at differences between control and VPA treated rats in cognitive attention tasks, and the associated neurobiological changes found in grey matter volumes of across the brain after exercise interventions. Additionally, we are using electrophysiology to record from the medial prefrontal cortex during cognitive performance in the Fmr1 knock out rat.  We are interested in understanding change across the life-span and have projects that examine adolescent development as well as aged animals.