Fragile X mental retardation protein in learning-related synaptic plasticity

Mol Cells. 2009 Dec 31;28(6):501-7. doi: 10.1007/s10059-009-0193-x. Epub 2009 Dec 23.


Fragile X syndrome (FXS) is caused by a lack of the fragile X mental retardation protein (FMRP) due to silencing of the Fmr1 gene. As an RNA binding protein, FMRP is thought to contribute to synaptic plasticity by regulating plasticity-related protein synthesis and other signaling pathways. Previous studies have mostly focused on the roles of FMRP within the hippocampus--a key structure for spatial memory. However, recent studies indicate that FMRP may have a more general contribution to brain functions, including synaptic plasticity and modulation within the prefrontal cortex. In this brief review, we will focus on recent studies reported in the prefrontal cortex, including the anterior cingulate cortex (ACC). We hypothesize that alterations in ACC-related plasticity and synaptic modulation may contribute to various forms of cognitive deficits associated with FXS.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Cognition Disorders / complications
  • Cognition Disorders / genetics*
  • Cognition Disorders / pathology
  • Cognition Disorders / physiopathology
  • Fragile X Mental Retardation Protein / physiology*
  • Fragile X Syndrome / complications
  • Fragile X Syndrome / genetics*
  • Fragile X Syndrome / pathology
  • Fragile X Syndrome / physiopathology
  • Humans
  • Learning / physiology*
  • Memory / physiology
  • Neuronal Plasticity
  • Prefrontal Cortex / pathology
  • Prefrontal Cortex / physiology*
  • Synaptic Transmission


  • Fragile X Mental Retardation Protein