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

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.

Pubmed ID: 7502080

Authors

  • Brusa R
  • Zimmermann F
  • Koh DS
  • Feldmeyer D
  • Gass P
  • Seeburg PH
  • Sprengel R

Journal

Science (New York, N.Y.)

Publication Data

December 8, 1995

Associated Grants

None

Mesh Terms

  • Alleles
  • Animals
  • Base Sequence
  • Calcium
  • Epilepsy
  • Gene Targeting
  • Glutamic Acid
  • Heterozygote
  • Hippocampus
  • In Situ Hybridization
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Molecular Sequence Data
  • Nerve Degeneration
  • Neurons
  • Polymerase Chain Reaction
  • Purkinje Cells
  • Pyramidal Cells
  • RNA Editing
  • RNA Precursors
  • Receptors, AMPA