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J Physiol Volume 586, Number 6, 1503-1508, March 15, 2008 DOI: 10.1113/jphysiol.2008.150722
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SYMPOSIUM REPORT

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

 Gül Dölen1,2 and Mark F. Bear1

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

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.

(Received 3 January 2008; accepted after revision 11 January 2007; first published online 17 January 2007)
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{at}mit.edu

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.




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