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EMBO reports 6, 1, 90–95 (2005)
doi:10.1038/sj.embor.7400312
Published online: 10 December 2004
Rescue of abnormal phenotypes of the  2 glutamate receptor-null mice by mutant 2 transgenes
Hirokazu Hirai1, 2, 3, Taisuke Miyazaki4, Wataru Kakegawa1, 5, Shinji Matsuda1, 5, Masayoshi Mishina6, Masahiko Watanabe4 & Michisuke Yuzaki1, 5
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1 Deptartment of Developmental Neurobiology, St Jude Children's Research Hospital, Memphis, Tennessee 38105, USA
2 Advanced Science Research Center, Kanazawa University, Kanazawa 920-8640, Japan
3 PRESTO, Japan Science and Technology Agency, Saitama 332-0012, Japan
4 Department of Anatomy, Hokkaido University School of Medicine, Sapporo 060-8638, Japan
5 Department of Physiology, Keio University School of Medicine, Tokyo 160-8582, Japan
6 Department of Molecular Neurobiology, School of Medicine, University of Tokyo, Tokyo 113-0033, Japan
To whom correspondence should be addressed
Michisuke Yuzaki Tel: +81 3 5363 3749; Fax: +81 3 3359 0437; E-mail: myuzaki@sc.itc.keio.ac.jp
Received 2 July 2004; Accepted 18 November 2004; Published online 10 December 2004.
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Abstract
The 2 glutamate receptor (GluR2) has a crucial role in cerebellar functions; disruption of GluR 2 alleles in mice (2-/-) impairs synapse formation and long-term depression, which is thought to underlie motor learning in the cerebellum, and consequently leads to motor discoordination. However, it has been unclear whether GluR2 is activated by glutamate analogues. Here we introduced a GluR2 transgene, which had a mutation (Arg514Lys) in the putative ligand-binding motif conserved in all mammalian ionotropic glutamate receptors (iGluRs) and their ancestral bacterial periplasmic amino-acid-binding proteins, into 2-/- mice. Surprisingly, a mutant GluR2 transgene, as well as a wild-type GluR2 transgene, rescued all abnormal phenotypes of 2-/- mice. Therefore, these results indicate that the conserved arginine residue, which is crucial for the binding of iGluRs to glutamate analogues, is not essential for the restoration of GluR2 functions in 2-/- mice.
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