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  Importance of the intracellular domain of NR2 subunits for NMDA receptor function in vivo

Sprengel, R., Suchanek, B., Amico, C., Brusa, R., Burnashev, N., Rozov, A., et al. (1998). Importance of the intracellular domain of NR2 subunits for NMDA receptor function in vivo. Cell, 92, 279-289. doi:10.1016/S0092-8674(00)80921-6.

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Genre: Journal Article
Alternative Title : Importance of the intracellular domain of NR2 subunits for NMDA receptor function in vivo

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 Creators:
Sprengel, Rolf1, Author           
Suchanek, Bettina1, Author           
Amico, Carla2, Author           
Brusa, Rossella1, Author           
Burnashev, Nail2, Author           
Rozov, Andrej1, 2, Author           
Hvalby, Øivind, Author
Jensen, Vidar, Author
Paulsen, Ole, Author
Andersen, Per, Author
Kim, Jeansok J., Author
Thompson, Richard F., Author
Sun, William, Author
Webster, Lorna C., Author
Grant, Seth G. N., Author
Eilers, Jens, Author
Konnerth, Arthur, Author
McNamara, James O., 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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 Abstract: NMDA receptors, a class of glutamate-gated cation channels with high Ca2+ conductance, mediate fast transmission and plasticity of central excitatory synapses. We show here that gene-targeted mice expressing NMDA receptors without the large intracellular C-terminal domain of any one of three NR2 subunits phenotypically resemble mice made deficient in that particular subunit. Mice expressing the NR2B subunit in a C-terminally truncated form (NR2B(deltaC/deltaC) mice) die perinatally. NR2A(deltaC/deltaC) mice are viable but exhibit impaired synaptic plasticity and contextual memory. These and NR2C(deltaC/deltaC) mice display deficits in motor coordination. C-terminal truncation of NR2 subunits does not interfere with the formation of gateable receptor channels that can be synaptically activated. Thus, the phenotypes of our mutants appear to reflect defective intracellular signaling.

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Language(s): eng - English
 Dates: 1997-12-091997-09-121997-12-091998-01-23
 Publication Status: Issued
 Pages: 11
 Publishing info: -
 Table of Contents: -
 Rev. Type: Peer
 Degree: -

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Title: Cell
Source Genre: Journal
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Publ. Info: Cambridge, Mass. : Cell Press
Pages: 2 Volume / Issue: 92 Sequence Number: - Start / End Page: 279 - 289 Identifier: ISSN: 0092-8674
CoNE: https://pure.mpg.de/cone/journals/resource/954925463183