The δ2 glutamate receptor: 10 Years later

研究成果: Article

89 引用 (Scopus)

抄録

The orphan glutamate receptor δ2 (GluRδ2) is predominantly expressed in Purkinje cells and plays a crucial role in cerebellar functions: mice that lack the GluRδ2 gene display ataxia and impaired synaptic plasticity. However, when expressed alone or with other glutamate receptors, GluRδ2 does not form functional glutamate-gated ion channels nor does it bind to glutamate analogs. Therefore, the mechanisms by which GluRδ2 participates in cerebellar functions have been elusive. Studies of mutant mice such as lurcher, hotfoot, and GluRδ2 knockout mice have provided clues to the structure and function of GluRδ2. GluRδ2 has a channel pore similar to that of other glutamate receptors; the channel is functional at least when the lurcher mutation is present. GluRδ2 must be transported to the Purkinje cell surface to function; the absence of surface GluRδ2 causes the ataxic phenotype of hotfoot mice. In GluRδ2-null mice, the presence of naked spines not innervated by parallel fibers may influence the sustained innervation of mutant Purkinje cells by multiple climbing fibers. From these results, several hypotheses about mechanisms by which GluRδ2 functions are proposed in this article. Further characterization of GluRδ2's functions will provide key insights into normal and abnormal cerebellar functions.

元の言語English
ページ(範囲)11-22
ページ数12
ジャーナルNeuroscience Research
46
発行部数1
DOI
出版物ステータスPublished - 2003 5 1
外部発表Yes

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Glutamate Receptors
Purkinje Cells
Glutamic Acid
Neuronal Plasticity
Ataxia
Ion Channels
Knockout Mice
Spine

ASJC Scopus subject areas

  • Neuroscience(all)

これを引用

The δ2 glutamate receptor : 10 Years later. / Yuzaki, Michisuke.

:: Neuroscience Research, 巻 46, 番号 1, 01.05.2003, p. 11-22.

研究成果: Article

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