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  Dysfunction in mice by NMDA receptor point mutations NR1(N598Q) and NR1(N598R)

Single, F. N., Rozov, A., Burnashev, N., Zimmermann, F., Hanley, D. F., Forrest, D., et al. (2000). Dysfunction in mice by NMDA receptor point mutations NR1(N598Q) and NR1(N598R). The Journal of Neuroscience: the Official Journal of the Society for Neuroscience, 20(7), 2558-2566. Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/10729336.

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Item Permalink: http://hdl.handle.net/11858/00-001M-0000-0028-2D67-F Version Permalink: http://hdl.handle.net/11858/00-001M-0000-0028-2D68-D
Genre: Journal Article
Alternative Title : Dysfunction in mice by NMDA receptor point mutations NR1(N598Q) and NR1(N598R)

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JNeurosci_20_2000_2558.pdf (Any fulltext), 385KB
 
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 Creators:
Single, Frank Nicolai1, Author              
Rozov, Andrej1, 2, Author              
Burnashev, Nail2, Author              
Zimmermann, Frank, Author
Hanley, Daniel F., Author
Forrest, Douglas, Author
Curran, Tom, Author
Jensen, Vidar, Author
Hvalby, Øivind, Author
Sprengel, Rolf1, Author              
Seeburg, Peter H.1, Author              
Affiliations:
1Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society, ou_1497704              
2Department of Cell Physiology, Max Planck Institute for Medical Research, Max Planck Society, ou_1497701              

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Free keywords: NMDA receptor gene targeting Cre-lox Mg2+block Ca2+ influx coincidence detection respiration nurturing barrel cortex LTP
 Abstract: NMDA receptors in mice were mutated by gene targeting to substitute asparagine (N) in position 598 of the NR1 subunit to glutamine (Q) or arginine (R). Animals expressing exclusively the mutated NR1 alleles, NR1(Q/Q) and NR1(-/R) mice, developed a perinatally lethal phenotype mainly characterized by respiratory failure. The dysfunctions were partially rescued in heterozygous mice by the presence of pure wild-type receptors. Thus, NR1(+/Q) mice exhibited reduced life expectancy, with females being impaired in nurturing; NR1(+/R) mice displayed signs of underdevelopment such as growth retardation and impaired righting reflex, and died before weaning. We analyzed the key properties of NMDA receptors, high Ca(2+) permeability, and voltage-dependent Mg(2+) block, in the mutant mice. Comparison of the complex physiological and phenotypical changes observed in the different mutants indicates that properties controlled by NR1 subunit residue N598 are important for autonomic brain functions at birth and during postnatal development. We conclude that disturbed NMDA receptor signaling mediates a variety of neurological phenotypes

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Language(s): eng - English
 Dates: 1999-09-142000-01-142000-04-01
 Publication Status: Published in print
 Pages: 9
 Publishing info: -
 Table of Contents: -
 Rev. Type: Peer
 Identifiers: eDoc: 666301
PMID: 10729336
URI: http://www.ncbi.nlm.nih.gov/pubmed/10729336
URI: http://www.jneurosci.org/content/20/7/2558.full
Other: 4820
 Degree: -

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Title: The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
  Other : J. Neurosci.
Source Genre: Journal
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Publ. Info: Baltimore, MD : The Society
Pages: - Volume / Issue: 20 (7) Sequence Number: - Start / End Page: 2558 - 2566 Identifier: ISSN: 0270-6474
CoNE: https://pure.mpg.de/cone/journals/resource/954925502187_1