Ca2+ permeability of the channel pore is not essential for the δ2 glutamate receptor to regulate synaptic plasticity and motor coordination

Wataru Kakegawa, Taisuke Miyazaki, Hirokazu Hirai, Junko Motohashi, Masayoshi Mishina, Masahiko Watanabe, Michisuke Yuzaki

Research output: Contribution to journalArticle

30 Citations (Scopus)

Abstract

The δ2 glutamate receptor (GluRδ2) plays a crucial role in cerebellar functions; mice with a disrupted GluR δ 2 gene (GluR δ 2-/-) display impaired synapse formation and abrogated long-term depression (LTD). However, the mechanisms by which GluRδ2 functions have remained unclear. Because a GluRδ2 mutation in lurcher mice causes channel activities characterized by Ca2+ permeability, GluRδ2 was previously suggested to serve as a Ca2+-permeable channel in Purkinje cells. To test this hypothesis, we introduced a GluRδ2 transgene, which had a mutation (Gln618Arg) in the putative channel pore, into GluRδ2-/- mice. Interestingly, the mutant transgene rescued the major functional and morphological abnormalities of GluRδ2-/- 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 GluRδ2.

Original languageEnglish
Pages (from-to)729-735
Number of pages7
JournalJournal of Physiology
Volume579
Issue number3
DOIs
Publication statusPublished - 2007 Mar 15

ASJC Scopus subject areas

  • Physiology

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