GRM5 and Anxiety: These data strongly support the hypothesis that modest over-expression of AβPP and/or Aβ, in the context of the Fmr1KO, is necessary for many of the pathological phenotypes including AGS, anxiety, dendritic dysmorphogenesis and mGluR-LTD observed in the mice and that these effects are likely mediated by mGluR5 signaling.