One of the crucial functions of astrocytes in the healthy brain is to maintain very low levels of the excitatory neurotransmitter, glutamate. This is accomplished by removal of excess glutamate through specialized glutamate transporters, such as GLT1, which are specifically found on astrocytes. Recently, we discovered that Fragile X Syndrome (FXS) mice have fewer and more dysfunctional GLT1 transporters. In this mini-grant we propose to expand on our findings in the rodent brain. We propose to evaluate human brain tissue samples to assess whether there is a similar alteration in human glutamate transporter in FXS and autism patients. This study will be the first to address whether human astrocyte dysfunction contributes to the development of FXS, and may identify an important new target for restoration of normal brain development in both FXS and autism patients.