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First published online on January 17, 2008.
 Copyright © 2008 by The Physiological Society
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jphysiol.2008.150722v1
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Gul Dolen
Mark F Bear
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Received January 3, 2008
Revised January 8, 2008
Accepted after revision January 11, 2008

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

Gul Dolen1 and Mark F Bear2*

1 HHMI, PILM, BCS, MIT and Brown University Medical School
2 HHMI, PCLM, BCS, MIT

* To whom correspondence should be addressed. E-mail: mbear{at}mit.edu.

Metabotropic glutamate receptors (mGluRs) have been implicated in a diverse variety of neuronal functions. Studies reviewed here indicate that exaggerated signaling through mGluR5 can account for multiple cognitive and syndromic features of fragile X syndrome, the most common inherited form of mental retardation and autism. Because a reduction of mGluR5 signaling 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.


Key words: Glutamate receptor • Memory • Synaptic plasticity • FMRP fragile X mental retardation protein • metabotropic glutamate receptor • protein synthesis




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