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J Physiol Volume 584, Number 1, 89-96, October 1, 2007 DOI: 10.1113/jphysiol.2007.141291
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RAPID REPORT

The {delta}2 ‘ionotropic’ glutamate receptor functions as a non-ionotropic receptor to control cerebellar synaptic plasticity

 Wataru Kakegawa1, Kazuhisa Kohda1 and Michisuke Yuzaki1

1 Department of Physiology, School of Medicine, Keio University, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan

The {delta}2 glutamate receptor (GluR{delta}2) belongs to the ionotropic glutamate receptor (iGluR) family and plays a crucial role in the induction of cerebellar long-term depression (LTD), a form of synaptic plasticity underlying motor learning. Nevertheless, the mechanisms by which GluR{delta}2 regulates cerebellar LTD have remained elusive. Because a mutation occurring in lurcher mice causes continuous GluR{delta}2 channel activity that can be abolished by 1-naphtylacetylspermine (NASP), a channel blocker for Ca2+-permeable iGluRs, GluR{delta}2 is thought to function as an ion channel. Here, we introduced a mutant GluR{delta}2 transgene, in which the putative channel pore was disrupted, into GluR{delta}2-null Purkinje cells using a virus vector. Surprisingly and similar to the effect of the wild-type GluR{delta}2 transgene, the mutant GluR{delta}2 completely rescued the abrogated LTD in GluR{delta}2-null mice. Furthermore, NASP did not block LTD induction in wild-type cerebellar slices. These results indicate that GluR{delta}2, a member of the iGluR family, does not serve as a channel in the regulation of LTD induction.

(Received 24 July 2007; accepted after revision 8 August 2007; first published online 16 August 2007)
Corresponding author M. Yuzaki: Department of Physiology, School of Medicine, Keio University, 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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