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ARTICLE, CELLULAR/MOLECULAR

Generation and Analysis of GluR5(Q636R) Kainate Receptor Mutant Mice

Andreas Sailer, Geoffrey T. Swanson, Isabel Pérez-Otaño, Lora O’Leary, Shelle A. Malkmus, Richard H. Dyck, Heather Dickinson-Anson, Hans H. Schiffer, Cornelia Maron, Tony L. Yaksh, Fred H. Gage, Stephen O’Gorman and Stephen F. Heinemann
Journal of Neuroscience 15 October 1999, 19 (20) 8757-8764; https://doi.org/10.1523/JNEUROSCI.19-20-08757.1999
Andreas Sailer
1 Molecular Neurobiology Laboratory,
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Geoffrey T. Swanson
1 Molecular Neurobiology Laboratory,
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Isabel Pérez-Otaño
1 Molecular Neurobiology Laboratory,
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Lora O’Leary
1 Molecular Neurobiology Laboratory,
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Shelle A. Malkmus
4Department of Pharmacology and Anesthesiology, University of California, San Diego, La Jolla, California 92093
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Richard H. Dyck
1 Molecular Neurobiology Laboratory,
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Heather Dickinson-Anson
3Laboratory of Genetics, The Salk Institute for Biological Studies, La Jolla, California 92037, and
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Hans H. Schiffer
1 Molecular Neurobiology Laboratory,
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Cornelia Maron
1 Molecular Neurobiology Laboratory,
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Tony L. Yaksh
4Department of Pharmacology and Anesthesiology, University of California, San Diego, La Jolla, California 92093
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Fred H. Gage
3Laboratory of Genetics, The Salk Institute for Biological Studies, La Jolla, California 92037, and
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Stephen O’Gorman
2Gene Expression Laboratory, and
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Stephen F. Heinemann
1 Molecular Neurobiology Laboratory,
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Abstract

The physiological significance of RNA editing of transcripts that code for kainate-preferring glutamate receptor subunits is unknown, despite the fact that the functional consequences of this molecular modification have been well characterized in cloned receptor subunits. RNA editing of the codon that encodes the glutamine/arginine (Q/R) site in the second membrane domain (MD2) of glutamate receptor 5 (GluR5) and GluR6 kainate receptor subunits produces receptors with reduced calcium permeabilities and single-channel conductances. Approximately 50% of the GluR5 subunit transcripts from adult rat brain are edited at the Q/R site in MD2. To address the role of glutamate receptor mRNA editing in the brain, we have made two strains of mice with mutations at amino acid 636, the Q/R-editing site in GluR5, using embryonic stem cell–mediated transgenesis. GluR5(RloxP/RloxP) mice encode an arginine at the Q/R site of the GluR5 subunit, whereas GluR5(wtloxP/wtloxP) mice encode a glutamine at this site, similar to wild-type mice. Mutant animals do not exhibit developmental abnormalities, nor do they show deficits in the behavioral paradigms tested in this study. Kainate receptor current densities were reduced by a factor of six in acutely isolated sensory neurons of dorsal root ganglia from GluR5(RloxP/RloxP) mice compared with neurons from wild-type mice. However, the editing mutant mice did not exhibit altered responses to thermal and chemical pain stimuli. Our investigations with the GluR5-editing mutant mice have therefore defined a set of physiological processes in which editing of the GluR5 subunit is unlikely to play an important role.

  • RNA editing
  • glutamate receptor
  • pain
  • dorsal root ganglia
  • gene targeting
  • Cre recombinase
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The Journal of Neuroscience: 19 (20)
Journal of Neuroscience
Vol. 19, Issue 20
15 Oct 1999
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Generation and Analysis of GluR5(Q636R) Kainate Receptor Mutant Mice
Andreas Sailer, Geoffrey T. Swanson, Isabel Pérez-Otaño, Lora O’Leary, Shelle A. Malkmus, Richard H. Dyck, Heather Dickinson-Anson, Hans H. Schiffer, Cornelia Maron, Tony L. Yaksh, Fred H. Gage, Stephen O’Gorman, Stephen F. Heinemann
Journal of Neuroscience 15 October 1999, 19 (20) 8757-8764; DOI: 10.1523/JNEUROSCI.19-20-08757.1999

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Generation and Analysis of GluR5(Q636R) Kainate Receptor Mutant Mice
Andreas Sailer, Geoffrey T. Swanson, Isabel Pérez-Otaño, Lora O’Leary, Shelle A. Malkmus, Richard H. Dyck, Heather Dickinson-Anson, Hans H. Schiffer, Cornelia Maron, Tony L. Yaksh, Fred H. Gage, Stephen O’Gorman, Stephen F. Heinemann
Journal of Neuroscience 15 October 1999, 19 (20) 8757-8764; DOI: 10.1523/JNEUROSCI.19-20-08757.1999
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Keywords

  • RNA editing
  • glutamate receptor
  • pain
  • dorsal root ganglia
  • gene targeting
  • Cre recombinase

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