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231224s2012 xx |||||o 00| ||eng c |
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|a 10.1155/2012/275630
|2 doi
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|a eng
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|a Martin, Brandon S
|e verfasserin
|4 aut
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|a Pathological plasticity in fragile X syndrome
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|c 2012
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|a Text
|b txt
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|a ƒaComputermedien
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|a ƒa Online-Ressource
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|a Date Completed 20.11.2012
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|a Date Revised 29.04.2023
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|a published: Print-Electronic
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|a Citation Status MEDLINE
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|a 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
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|a Journal Article
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|a Research Support, N.I.H., Extramural
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|a Research Support, Non-U.S. Gov't
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|a Review
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|a Adaptor Proteins, Signal Transducing
|2 NLM
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|a CYFIP1 protein, human
|2 NLM
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|a Receptors, Cannabinoid
|2 NLM
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|a Receptors, Glutamate
|2 NLM
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|a Fragile X Mental Retardation Protein
|2 NLM
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|a 139135-51-6
|2 NLM
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1 |
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|a Huntsman, Molly M
|e verfasserin
|4 aut
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| 773 |
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|i Enthalten in
|t Neural plasticity
|d 1998
|g 2012(2012) vom: 15., Seite 275630
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|x 1687-5443
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| 773 |
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|g volume:2012
|g year:2012
|g day:15
|g pages:275630
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| 856 |
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|u http://dx.doi.org/10.1155/2012/275630
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