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Science. 1995 Dec 8;270(5242):1677-80.

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

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  • 1Laboratory of Molecular Neuroendocrinology, University of Heidelberg, Germany.

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.

PMID:
7502080
[PubMed - indexed for MEDLINE]
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