Because of autism is a complex neurobiological disorder with multiple causes, it has been useful to develop animal models that recapitulate only some of the symptoms of the disorder to isolate specific genes of interest and their influence on the spectrum of behavioral disturbances. Fragile X and Rett Syndrome are two neurodevelopmental disorders that result in mental retardation and autistic behavior. Each of these disorders is caused by the disruption of a single gene and therefore it has been possible to generate a model of the human disease by genetic mutation in mice. The mouse models for these two syndromes display many of the same traits as the human disease, including some neurobiological and neuropathological correlates. This study will record activity from individual neurons in the somatosensory region of Fragile X and Rett Syndrome mice in order to examine the precise nature of the deficits in synaptic communication and plasticity that are thought to underlie some of the cognitive dysfunctions of these two disorders. Significance: Studies which investigate the neurobiology of neurodevelomental disorders with known genetic causes provide a simple model for scientist to investigate the role of genes on brain development. The outlined research will give insight into fundamental disruptions in synaptic communication that may underlie the sensory and cognitive impairments in these mouse models and therefore enhance our understanding of the basis for the human disorders.