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J Physiol Volume 579, Number 3, 729-735, March 15, 2007 DOI: 10.1113/jphysiol.2006.127100
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RAPID REPORT

Ca2+ permeability of the channel pore is not essential for the {delta}2 glutamate receptor to regulate synaptic plasticity and motor coordination

 Wataru Kakegawa1, Taisuke Miyazaki2, Hirokazu Hirai3,4, Junko Motohashi1, Masayoshi Mishina5, Masahiko Watanabe2 and Michisuke Yuzaki1

1 Department of Physiology, School of Medicine, Keio University, Tokyo 160-8582, Japan
2 Department of Anatomy, Hokkaido University Graduate School of Medicine, Sapporo 060-8638, Japan
3 Department of Neurophysiology, Gunma University Graduate School of Medicine, Maebashi 371-8511, Japan
4 SORST, Japan Science and Technology Agency, Kawaguchi 332-0012, Japan
5 Department of Molecular Neurobiology and Pharmacology, Graduate School of Medicine, University of Tokyo, Tokyo 113-0033, Japan

The {delta}2 glutamate receptor (GluR{delta}2) plays a crucial role in cerebellar functions; mice with a disrupted GluR{delta}2 gene (GluR{delta}2–/–) display impaired synapse formation and abrogated long-term depression (LTD). However, the mechanisms by which GluR{delta}2 functions have remained unclear. Because a GluR{delta}2 mutation in lurcher mice causes channel activities characterized by Ca2+ permeability, GluR{delta}2 was previously suggested to serve as a Ca2+-permeable channel in Purkinje cells. To test this hypothesis, we introduced a GluR{delta}2 transgene, which had a mutation (Gln618Arg) in the putative channel pore, into GluR{delta}2–/– mice. Interestingly, the mutant transgene rescued the major functional and morphological abnormalities of GluR{delta}2–/– Purkinje cells, such as enhanced paired-pulse facilitation, impaired LTD at parallel fibre synapses, and sustained innervation by multiple climbing fibres. These results indicate that the conserved glutamine residue in the channel pore, which is crucial for all Ca2+-permeable glutamate receptors, is not essential for the function of GluR{delta}2.

(Received 20 December 2006; accepted after revision 18 January 2007; first published online 25 January 2007)
Corresponding author M. Yuzaki: Department of Physiology, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan. Email: myuzaki{at}sc.itc.keio.ac.jp

This paper has online supplemental material.




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