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Mutation in hotfoot‐4J mice results in retention of δ2 glutamate receptors in ER by Shinji Matsuda; Michisuke Yuzaki is a Neuroscience article available to read on EtoBox.

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## Abstract The orphan glutamate receptor δ2 is selectively expressed in Purkinje cells and plays a critical role in cerebellar function. Recently, the ataxia of __hotfoot‐4J__ (__ho‐4J__) mice was shown to be caused by a 170–amino acid deletion in the N‐terminal region of δ2 receptors. To understand δ2 receptor function, we characterized these mutant receptors (δ2^ho^) in Purkinje cells. Immunohistochemical staining showed that δ2^ho^ receptors of the __ho‐4J__ homozygotes were abundantly expressed but localized to the Purkinje cell soma; in wild‐type mice, δ2 receptors were predominantly present at distal dendrites of Purkinje cells. In addition, δ2^ho^ receptors of the __ho‐4J__ mice were sensitive to endoglycosidase H, a finding suggesting that δ2^ho^ receptors were not transported beyond the endoplasmic reticulum (ER) or __cis__‐Golgi apparatus. To gain further insights into the mechanisms of this phenomenon, we characterized δ2^ho^ receptors in transfected HEK293 cells. δ2^ho^ receptors expressed in HEK293 cells were also sensitive to endoglycosidase H. Immunohistochemical staining showed that δ2^ho^ receptors colocalized with proteins retained in the ER. Furthermore, δ2^ho^

Who reads Mutation in hotfoot‐4J mice results in retention of δ2 glutamate receptors in ER?

Author

Shinji Matsuda; Michisuke Yuzaki

Publisher

John Wiley and Sons; Wiley (Blackwell Publishing); Blackwell Publishing Inc.; Wiley (ISSN 0953-816X)

Published

2002

Language

EN

Field

Neuroscience (Life Sciences)