Molecular Neurobiology

, Volume 39, Issue 2, pp 107–129

The Fragile X Mental Retardation Protein in Circadian Rhythmicity and Memory Consolidation

Article

DOI: 10.1007/s12035-009-8057-0

Cite this article as:
Gatto, C.L. & Broadie, K. Mol Neurobiol (2009) 39: 107. doi:10.1007/s12035-009-8057-0

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.

Keywords

Fragile X syndromeLearningMemoryCircadian rhythmMushroom bodyClock circuitNeuronAxonDendriteSynapseDrosophila

Copyright information

© Humana Press Inc. 2009

Authors and Affiliations

  1. 1.Department of Biological Sciences, Kennedy Center for Research on Human DevelopmentVanderbilt UniversityNashvilleUSA