The changing nature of synaptic function in neuronal dendrites during development is one of a myriad of phenomenological observations that have fascinated neurobiologists for some time. In the case of fragile X syndrome (FXS), neurons exhibit long, spindly dendritic spines that appear to be morphologically immature (1). As with all dendritic spines, these FXR spines typically house elements of the postsynaptic density juxtaposed with components of the translation apparatus (2). A dominant mutation in the FMR1 gene gives rise to FXS through the elimination of FMR1 RNA. This gene encodes the fragile X mental retardation protein (FMRP), which is a RNA-binding protein. By using in vitro assays, FMRP has been proposed to be involved in modulating translation through its binding to cellular RNAs and ribosomes (3). In early studies, Weiler et al. (4) showed that the FMR1 RNA was localized in dendrites and that its translation could be modulated by group 1 metabotropic glutamate receptor (Gp1 mGluR) agonists. Subsequent studies have extended, and begun to clarify, the potential aftereffects of such events and their impact on normal cellular functioning, as well as FXS. In this issue of PNAS, Weiler et al. (5) have taken an important step in showing the complexity of FMRP-mediated translational control. By using cortical synaptoneurosome preparations, Weiler et al. (5) demonstrate that Gp1 mGluR (i.e., mGluR1 and mGluR5) activation has …