| Synaptic ionotropic glutamate receptors and plasticity are developmentally altered in the CA1 field of Fmr1 knockout mice. | |
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MedLine Citation:
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PMID: 19103683 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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Yair Pilpel; Aleksander Kolleker; Sven Berberich; Melanie Ginger; Andreas Frick; Edwin Mientjes; Ben A Oostra; Peter H Seeburg |
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Publication Detail:
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Type: Comparative Study; Journal Article; Research Support, Non-U.S. Gov't Date: 2008-12-22 |
Journal Detail:
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Title: The Journal of physiology Volume: 587 ISSN: 1469-7793 ISO Abbreviation: J. Physiol. (Lond.) Publication Date: 2009 Feb |
Date Detail:
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Created Date: 2009-02-16 Completed Date: 2009-12-07 Revised Date: 2010-09-23 |
Medline Journal Info:
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Nlm Unique ID: 0266262 Medline TA: J Physiol Country: England |
Other Details:
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Languages: eng Pagination: 787-804 Citation Subset: IM |
Affiliation:
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Max Planck Institute for Medical Research, Department of Molecular Neurobiology, Heidelberg, Germany. yair.pilpel@mpimf-heidelberg.mpg.de |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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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:
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0/Receptors, AMPA; 0/Receptors, Glutamate; 0/Receptors, N-Methyl-D-Aspartate; 139135-51-6/Fragile X Mental Retardation Protein |
| Comments/Corrections | |
Comment In:
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J Physiol. 2009 Feb 15;587(Pt 4):723
[PMID:
19218622
]
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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