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Glutamate Receptor δ2 Is Essential for Input Pathway-Dependent Regulation of Synaptic AMPAR Contents in Cerebellar Purkinje Cells

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タイトル: Glutamate Receptor δ2 Is Essential for Input Pathway-Dependent Regulation of Synaptic AMPAR Contents in Cerebellar Purkinje Cells
著者: Yamasaki, Miwako 著作を一覧する
Miyazaki, Taisuke 著作を一覧する
Azechi, Hirotsugu 著作を一覧する
Abe, Manabu 著作を一覧する
Natsume, Rie 著作を一覧する
Hagiwara, Teruki 著作を一覧する
Aiba, Atsu 著作を一覧する
Mishina, Masayoshi 著作を一覧する
Sakimura, Kenji 著作を一覧する
Watanabe, Masahiko 著作を一覧する
発行日: 2011年 3月 2日
出版者: Society for Neuroscience
誌名: The Journal of Neuroscience
巻: 31
号: 9
開始ページ: 3362
終了ページ: 3374
出版社 DOI: 10.1523/JNEUROSCI.5601-10.2011
抄録: The number of synaptic AMPA receptors (AMPARs) is the major determinant of synaptic strength and is differently regulated in input pathway-dependent and target cell type-dependent manners. In cerebellar Purkinje cells (PCs), the density of synaptic AMPARs is approximately five times lower at parallel fiber (PF) synapses than at climbing fiber (CF) synapses. However, molecular mechanisms underlying this biased synaptic distribution remain unclear. As a candidate molecule, we focused on glutamate receptor δ2 (GluRδ2 or GluD2), which is known to be efficiently trafficked to and selectively expressed at PF synapses in PCs. We applied postembedding immunogold electron microscopy to GluRδ2 knock-out (KO) and control mice, and measured labeling density for GluA1-4 at three excitatory synapses in the cerebellar molecular layer. In both control and GluRδ2-KO mice, GluA1-3 were localized at PF and CF synapses in PCs, while GluA2-4 were at PF synapses in interneurons. In control mice, labeling density for each of GluA1-3 was four to six times lower at PF-PC synapses than at CF-PC synapses. In GluRδ2-KO mice, however, their labeling density displayed a three- to fivefold increase at PF synapses, but not at CF synapses, thus effectively eliminating input pathway-dependent disparity between the two PC synapses. Furthermore, we found an unexpected twofold increase in labeling density for GluA2 and GluA3, but not GluA4, at PF-interneuron synapses, where we identified low but significant expression of GluRδ2. These results suggest that GluRδ2 is involved in a common mechanism that restricts the number of synaptic AMPARs at PF synapses in PCs and molecular layer interneurons.
資料タイプ: article
URI: http://hdl.handle.net/2115/47052
出現コレクション:雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

提供者: 渡邉 雅彦

 

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