Tuberous sclerosis complex (TSC) and fragile X syndrome (FXS) are known risk factors for autism, and recently, the gene products that are mutated in TSC and FXS have been shown to be involved in the regulation of protein synthesis, which is important for memory formation. Thus, it is possible that aberrant regulation of protein synthesis in brain cells may contribute to the development of autism. In an experimental mouse model in which the TSC gene has been genetically modified over the entire life span (including embryonic development), abnormalities in brain development are seen which are similar to those in people with TSC. This approach does not distinguish the critical period (i.e. pre- or post-natally) in which the abnormal TSC gene exerts its effect. The present study will use a TSC mouse model to examine the relationship between brain abnormalities and behavioral and cognitive impairments and will specifically address what happens when the abnormality in the TSC gene is induced only in the post-natal period (i.e., after birth and thereby bypassing any effects on brain development).