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Significance Fragile X syndrome (FXS) is caused by loss of expression of fragile X mental retardation protein (FMRP), an RNA-binding protein that has been proposed to regulate local stimulus-dependent protein synthesis. However, how FMRP loss affects distributions of newly synthesized proteins remains unclear. Here, we report that local BDNF application promotes persistent accumulation of new PSD95 at stimulated synapses and dendrites, and that this accumulation is absent in FMRP-deficient mouse neurons. We further identify signaling pathways important for the protein synthesis abnormalities. These results provide direct evidence for deficits in local protein synthesis and accumulation in response to local stimulation in FXS, and support mTORC1-S6K1 pathway inhibition as a potential therapeutic approach for FXS.

Kinase pathway inhibition restores PSD95 induction in neurons lacking fragile X mental retardation protein