Abstract
The control of new protein synthesis provides a means to locally regulate the availability of synaptic components necessary for dynamic neuronal processes. The fragile X mental retardation protein (FMRP), an RNA-binding translational regulator, is a key player mediating appropriate synaptic protein synthesis in response to neuronal activity levels. Loss of FMRP causes fragile X syndrome (FraX), the most commonly inherited form of mental retardation and autism spectrum disorders. FraX-associated translational dysregulation causes wide-ranging neurological deficits including severe impairments of biological rhythms, learning processes, and memory consolidation. Dysfunction in cytoskeletal regulation and synaptic scaffolding disrupts neuronal architecture and functional synaptic connectivity. The understanding of this devastating disease and the implementation of meaningful treatment strategies require a thorough exploration of the temporal and spatial requirements for FMRP in establishing and maintaining neural circuit function.