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

MPS-Authors
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Feldmeyer,  Dirk
Department of Cell Physiology, Max Planck Institute for Medical Research, Max Planck Society;

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Brusa,  Rossella
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;

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Kornau,  Hans Christian
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;

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Rozov,  Andrej
Department of Cell Physiology, Max Planck Institute for Medical Research, Max Planck Society;
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;

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Burnashev,  Nail
Department of Cell Physiology, Max Planck Institute for Medical Research, Max Planck Society;

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Sprengel,  Rolf
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;

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Seeburg,  Peter H.
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;

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Citation

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.


Cite as: http://hdl.handle.net/11858/00-001M-0000-0024-6069-E
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