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Journal Article

Early-onset epilepsy and postnatal lethality associated with an editing-deficient GluR-B allele in mice.

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

/persons/resource/persons93833

Koh,  Duk Su
Department of Cell Physiology, Max Planck Institute for Medical Research, Max Planck Society;

/persons/resource/persons92876

Feldmeyer,  Dirk
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;

External Resource

https://www.sciencemag.org/content/270/5242/1677.full.pdf
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http://dx.doi.org/10.1126/science.270.5242.1677
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Citation

Brusa, R., Zimmermann, F., Koh, D. S., Feldmeyer, D., Gass, P., Seeburg, P. H., et al. (1995). Early-onset epilepsy and postnatal lethality associated with an editing-deficient GluR-B allele in mice. Science, 270(5242), 1677-1680. doi:10.1126/science.270.5242.1677.


Cite as: https://hdl.handle.net/11858/00-001M-0000-0024-21C6-E
Abstract
The arginine residue at position 586 of the GluR-B subunit renders heteromeric alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA)-sensitive glutamate receptor channels impermeable to calcium. The codon for this arginine is introduced at the precursor messenger RNA (pre-mRNA) stage by site-selective adenosine editing of a glutamine codon. Heterozygous mice engineered by gene targeting to harbor an editing-incompetent GluR-B allele synthesized unedited GluR-B subunits and, in principal neurons and interneurons, expressed AMPA receptors with increased calcium permeability. These mice developed seizures and died by 3 weeks of age, showing that GluR-B pre-mRNA editing is essential for brain function.