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Therapeutic implications of the mGluR theory of fragile X mental retardation

  1. M. F. Bear*

Article first published online: 2 JUN 2005

DOI: 10.1111/j.1601-183X.2005.00135.x

Issue

Genes, Brain and Behavior

Genes, Brain and Behavior

Volume 4, Issue 6, pages 393–398, August 2005

Additional Information

How to Cite

Bear, M. F. (2005), Therapeutic implications of the mGluR theory of fragile X mental retardation. Genes, Brain and Behavior, 4: 393–398. doi: 10.1111/j.1601-183X.2005.00135.x

Author Information

  1. The Picower Center for Learning and Memory, Howard Hughes Medical Institute and Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA, USA

*M. F. Bear, The Picower Center for Learning and Memory, Howard Hughes Medical Institute and Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. E-mail: mbear@mit.edu

Publication History

  1. Issue published online: 2 JUN 2005
  2. Article first published online: 2 JUN 2005
  3. Received 24 December 2004, revised 14 February 2005, accepted for publication 16 February 2005

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Keywords:

  • Anxiety disorder;
  • autism;
  • cognitive development;
  • dendritic protein synthesis;
  • long-term depression;
  • metabotropic glutamate receptors;
  • seizure disorder

Evidence is reviewed that the consequences of group 1 metabotropic glutamate receptor (Gp1 mGluR) activation are exaggerated in the absence of the fragile X mental retardation protein, likely reflecting altered dendritic protein synthesis. Abnormal mGluR signaling could be responsible for remarkably diverse psychiatric and neurological symptoms in fragile X syndrome, including delayed cognitive development, seizures, anxiety, movement disorders and obesity.

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