Fragile X syndrome (FXS) is the most common inherited form of mental retardation and is caused by loss of function mutations in the Fragile X Mental Retardation gene (FMR1). Patients with FXS, as well as other forms of mental retardation, have an excess of dendritic spines as well as longer spines, suggesting that abnormal postsynaptic function, development, or plasticity contributes to the cognitive deficits of this disease. Fragile X Mental Retardation Protein (FMRP), the protein product of FMR1, regulates synapse development and plasticity, but precisely how this occurs is unknown. In this study, investigators will examine the cellular mechanisms by which FMRP regulates synapse development and plasticity. In particular, experiments will help determine how FMRP regulates the synaptic metabotropic glutamate receptor (mGluR), a molecule which holds promise as a therapeutic target for FXS and other autism spectrum disorders (ASDs). These results will help to determine the neurobiological basis of mental retardation and related disorders such as autism as well as test if mGluR antagonists are a suitable therapeutic strategy for FXS.