Document Detail


Synaptic ionotropic glutamate receptors and plasticity are developmentally altered in the CA1 field of Fmr1 knockout mice.
MedLine Citation:
PMID:  19103683     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Fragile X syndrome is one of the most common forms of mental retardation, yet little is known about the physiological mechanisms causing the disease. In this study, we probed the ionotropic glutamate receptor content in synapses of hippocampal CA1 pyramidal neurons in a mouse model for fragile X (Fmr1 KO2). We found that Fmr1 KO2 mice display a significantly lower AMPA to NMDA ratio than wild-type mice at 2 weeks of postnatal development but not at 6-7 weeks of age. This ratio difference at 2 weeks postnatally is caused by down-regulation of the AMPA and up-regulation of the NMDA receptor components. In correlation with these changes, the induction of NMDA receptor-dependent long-term potentiation following a low-frequency pairing protocol is increased in Fmr1 KO2 mice at this developmental stage but not later in maturation. We propose that ionotropic glutamate receptors, as well as potentiation, are altered at a critical time point for hippocampal network development, causing long-term changes. Associated learning and memory deficits would contribute to the fragile X mental retardation phenotype.
Authors:
Yair Pilpel; Aleksander Kolleker; Sven Berberich; Melanie Ginger; Andreas Frick; Edwin Mientjes; Ben A Oostra; Peter H Seeburg
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't     Date:  2008-12-22
Journal Detail:
Title:  The Journal of physiology     Volume:  587     ISSN:  1469-7793     ISO Abbreviation:  J. Physiol. (Lond.)     Publication Date:  2009 Feb 
Date Detail:
Created Date:  2009-02-16     Completed Date:  2009-12-07     Revised Date:  2010-09-23    
Medline Journal Info:
Nlm Unique ID:  0266262     Medline TA:  J Physiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  787-804     Citation Subset:  IM    
Affiliation:
Max Planck Institute for Medical Research, Department of Molecular Neurobiology, Heidelberg, Germany. yair.pilpel@mpimf-heidelberg.mpg.de
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MeSH Terms
Descriptor/Qualifier:
Animals
Animals, Newborn
Fragile X Mental Retardation Protein / biosynthesis,  genetics*
Gene Expression Regulation, Developmental / genetics*
Hippocampus / metabolism,  pathology
Long-Term Potentiation / genetics
Mice
Mice, Inbred C57BL
Mice, Knockout
Neuronal Plasticity / genetics*
Receptors, AMPA / metabolism
Receptors, Glutamate / metabolism*
Receptors, N-Methyl-D-Aspartate / metabolism
Synapses / genetics,  metabolism*,  pathology
Chemical
Reg. No./Substance:
0/Receptors, AMPA; 0/Receptors, Glutamate; 0/Receptors, N-Methyl-D-Aspartate; 139135-51-6/Fragile X Mental Retardation Protein
Comments/Corrections
Comment In:
J Physiol. 2009 Feb 15;587(Pt 4):723   [PMID:  19218622 ]

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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