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Neural Plasticity
Volume 2012, Article ID 275630, 12 pages
Review Article

Pathological Plasticity in Fragile X Syndrome

1Center for Neuroscience Research, Children's National Medical Center, Washington, DC 20010, USA
2Interdisciplinary Program in Neuroscience, Georgetown University Medical Center, Washington, DC 20057, USA

Received 9 March 2012; Accepted 21 May 2012

Academic Editor: Laurie C. Doering

Copyright © 2012 Brandon S. Martin and Molly M. Huntsman. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Deficits in neuronal plasticity are common hallmarks of many neurodevelopmental disorders. In the case of fragile-X syndrome (FXS), disruption in the function of a single gene, FMR1, results in a variety of neurological consequences directly related to problems with the development, maintenance, and capacity of plastic neuronal networks. In this paper, we discuss current research illustrating the mechanisms underlying plasticity deficits in FXS. These processes include synaptic, cell intrinsic, and homeostatic mechanisms both dependent on and independent of abnormal metabotropic glutamate receptor transmission. We place particular emphasis on how identified deficits may play a role in developmental critical periods to produce neuronal networks with permanently decreased capacity to dynamically respond to changes in activity central to learning, memory, and cognition in patients with FXS. Characterizing early developmental deficits in plasticity is fundamental to develop therapies that not only treat symptoms but also minimize the developmental pathology of the disease.