Role for metabotropic glutamate receptor 5 (mGluR5) in the pathogenesis of fragile X syndrome

Authors

  • Gül Dölen,

    1. Howard Hughes Medical Institute, The Picower Institute for Learning and Memory, Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA, USA
    2. Brown Medical School, Providence, RI, USA
    Search for more papers by this author
  • Mark F. Bear

    1. Howard Hughes Medical Institute, The Picower Institute for Learning and Memory, Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA, USA
    Search for more papers by this author

  • This report was presented at The Journal of Physiology Symposium on Synaptic Plasticity, San Diego, CA, USA, 2 November 2007. It was commissioned by the Editorial Board and reflects the views of the author.

Corresponding author M. F. Bear: Howard Hughes Medical Institute, The Picower Institute for Learning and Memory, Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA, USA. Email: mbear@mit.edu

Abstract

Metabotropic glutamate receptors (mGluRs) have been implicated in a diverse variety of neuronal functions. Studies reviewed here indicate that exaggerated signalling through mGluR5 can account for multiple cognitive and syndromic features of fragile X syndrome, the most common inherited form of mental retardation and autism. Since a reduction of mGluR5 signalling can reverse fragile X phenotypes, these studies provide a compelling rationale for the use of mGluR5 antagonists for the treatment of fragile X and related disorders.

Ancillary