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NMDA receptors are expressed in developing oligodendrocyte processes and mediate injury

机译：NMDA受体在发育中的少突胶质细胞过程中表达并介导损伤

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摘要

Injury to oligodendrocyte processes, the structures responsible for myelination, is implicated in many forms of brain disorder. Here we show NMDA (N-methyl-D-aspartate) receptor subunit expression on oligodendrocyte processes, and the presence of NMDA receptor subunit messenger RNA in isolated white matter. NR1, NR2A, NR2B, NR2C, NR2D and NR3A subunits showed clustered expression in cell processes, but NR3B was absent. During modelled ischaemia, NMDA receptor activation resulted in rapid Ca~(2+)-dependent detachment and disintegration of oligo-dendroglial processes in the white matter of mice expressing green fluorescent protein (GFP) specifically in oligodendrocytes (CNP-GFP mice). This effect occurred at mouse ages corresponding to both the initiation and the conclusion of myelination. NR1 subunits were found mainly in oligodendrocyte processes, whereas AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazole propio-nic acid)/kainate receptor subunits were mainly found in the somata. Consistent with this observation, injury to the somata was prevented by blocking AMPA/kainate receptors, and preventing injury to oligodendroglial processes required the blocking of NMDA receptors. The presence of NMDA receptors in oligodendrocyte processes explains why previous studies that have focused on the somata have not detected a role for NMDA receptors in oligodendrocyte injury. These NMDA receptors bestow a high sensitivity to acute injury and represent an important new target for drug development in a variety of brain disorders.
机译：少突胶质细胞过程（负责髓鞘形成的结构）的损伤与多种形式的脑部疾病有关。在这里，我们显示了少突胶质细胞过程中NMDA（N-甲基-D-天冬氨酸）受体亚基的表达，以及分离的白质中NMDA受体亚基信使RNA的存在。 NR1，NR2A，NR2B，NR2C，NR2D和NR3A亚基在细胞过程中显示成簇表达，但不存在NR3B。在模型性局部缺血期间，NMDA受体激活导致特定于少突胶质细胞（CNP-GFP小鼠）的表达绿色荧光蛋白（GFP）的小鼠白质中Ca-（2+）依赖的少突胶质细胞突脱离和崩解。这种效应发生在与髓鞘形成的开始和结束都相对应的小鼠年龄。 NR1亚基主要存在于少突胶质细胞过程中，而AMPA（α-氨基-3-羟基-5-甲基-4-异恶唑丙酸）/海藻酸酯受体亚基主要存在于躯体中。与该观察结果一致，通过阻断AMPA /海藻酸酯受体可以预防对躯体的损伤，而需要阻断NMDA受体来预防对少突胶质突的损伤。少突胶质细胞过程中NMDA受体的存在解释了为什么以前集中在躯体上的研究没有发现NMDA受体在少突胶质细胞损伤中的作用。这些NMDA受体对急性损伤具有高度敏感性，并代表了各种脑部疾病药物开发的重要新目标。

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  • 来源
    《Nature》 |2005年第7071期|p.1167-1171|共5页
  • 作者

    Michael G. Salter; Robert Fern;

  • 作者单位

    Department of Cell Physiology and Pharmacology, University of Leicester, Leicester LE1 9HN, UK;

  • 收录信息 美国《科学引文索引》(SCI);美国《工程索引》(EI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 自然科学总论;
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