| Fragile X syndrome and the amygdala. | |
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MedLine Citation:
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PMID: 21555214 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
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Fragile X syndrome (FXS) is the most commonly inherited form of mental impairment and autism. Current understanding of the molecular and cellular mechanisms underlying FXS symptoms is derived mainly from studies on the hippocampus and cortex. However, FXS is also associated with strong emotional symptoms, which are likely to involve changes in the amygdala. Unfortunately, the synaptic basis of amygdalar dysfunction in FXS remains largely unexplored. Here we describe recent findings from mouse models of FXS that have identified synaptic defects in the basolateral amygdala that are in many respects distinct from those reported earlier in the hippocampus. Long-term potentiation and surface expression of AMPA-receptors are impaired. Further, presynaptic defects are seen at both excitatory and inhibitory synapses. Remarkably, some of these synaptic defects in the amygdala are also amenable to pharmacological rescue. These results also underscore the need to modify the current hippocampus-centric framework to better explain FXS-related synaptic dysfunction in the amygdala. |
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Authors:
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Aparna Suvrathan; Sumantra Chattarji |
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Publication Detail:
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Type: JOURNAL ARTICLE Date: 2011-5-7 |
Journal Detail:
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Title: Current opinion in neurobiology Volume: - ISSN: 1873-6882 ISO Abbreviation: - Publication Date: 2011 May |
Date Detail:
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Created Date: 2011-5-10 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 9111376 Medline TA: Curr Opin Neurobiol Country: - |
Other Details:
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Languages: ENG Pagination: - Citation Subset: - |
Copyright Information:
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Copyright © 2011 Elsevier Ltd. All rights reserved. |
Affiliation:
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National Center for Biological Sciences, Bangalore 560065, India. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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