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  Neurological dysfunctions in mice expressing different levels of the Q/R site-unedited AMPAR subunit GluR-B

Feldmeyer, D., Kask, K., Brusa, R., Kornau, H. C., Kolhekar, R., Rozov, A., et al. (1999). Neurological dysfunctions in mice expressing different levels of the Q/R site-unedited AMPAR subunit GluR-B. Nature Neuroscience, 2(2), 57-64. doi:10.1038/4561.

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Item Permalink: https://hdl.handle.net/11858/00-001M-0000-0024-6069-E Version Permalink: https://hdl.handle.net/11858/00-001M-0000-002D-A9CF-8
Genre: Journal Article

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NatNeurosci_2_1999_57.pdf (Any fulltext), 410KB
 
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http://www.nature.com/neuro/journal/v2/n1/pdf/nn0199_57.pdf (Any fulltext)
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http://dx.doi.org/10.1038/4561 (Any fulltext)
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 Creators:
Feldmeyer, Dirk1, Author           
Kask, Kalev, Author
Brusa, Rossella2, Author           
Kornau, Hans Christian2, Author           
Kolhekar, Rohini, Author
Rozov, Andrej1, 2, Author           
Burnashev, Nail1, Author           
Jensen, Vidar, Author
Hvalby, Øivind, Author
Sprengel, Rolf2, Author           
Seeburg, Peter H.2, Author           
Affiliations:
1Department of Cell Physiology, Max Planck Institute for Medical Research, Max Planck Society, ou_1497701              
2Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society, ou_1497704              

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 Abstract: We generated mouse mutants with targeted AMPA receptor (AMPAR) GluR-B subunit alleles, functionally expressed at different levels and deficient in Q/R-site editing. All mutant lines had increased AMPAR calcium permeabilities in pyramidal neurons, and one showed elevated macroscopic conductances of these channels. The AMPAR-mediated calcium influx induced NMDA-receptor-independent long-term potentiation (LTP) in hippocampal pyramidal cell connections. Calcium-triggered neuronal death was not observed, but mutants had mild to severe neurological dysfunctions, including epilepsy and deficits in dendritic architecture. The seizure-prone phenotype correlated with an increase in the macroscopic conductance, as independently revealed by the effect of a transgene for a Q/R-site-altered GluR-B subunit. Thus, changes in GluR-B gene expression and Q/R site editing can affect critical architectural and functional aspects of excitatory principal neurons

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Language(s): eng - English
 Dates: 1998-08-251998-11-091999-01-01
 Publication Status: Issued
 Pages: 8
 Publishing info: -
 Table of Contents: -
 Rev. Type: Peer
 Identifiers: eDoc: 666542
DOI: 10.1038/4561
URI: http://www.ncbi.nlm.nih.gov/pubmed/10195181
URI: http://www.nature.com/neuro/journal/v2/n1/full/nn0199_57.html
URI: http://www.nature.com/neuro/journal/v2/n1/pdf/nn0199_57.pdf
Other: 4402
 Degree: -

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Title: Nature Neuroscience
  Other : Nat. Neurosci.
Source Genre: Journal
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Publ. Info: New York, NY : Nature America Inc.
Pages: - Volume / Issue: 2 (2) Sequence Number: - Start / End Page: 57 - 64 Identifier: ISSN: 1097-6256
CoNE: https://pure.mpg.de/cone/journals/resource/954925610931