GRM5 and fragile X syndrome: Numerous studies support the “mGluR theory of FXS” that suggests enhanced group 1 metabotropic glutamate receptor 5 (mGluR5) signaling is responsible for deficits in synaptogenesis, dendritic spine morphology, long-term potentiation (LTP) and depression (LTD) in the disease state [5, 27, 28, 30–32, 34–43].