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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Dependence of nodal sodium channel clustering on paranodal axoglial contact in the developing CNS.
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Dependence of nodal sodium channel clustering on paranodal axoglial contact in the developing CNS.

机译：发育中的中枢神经系统中淋巴结钠离子通道簇对结旁神经胶质接触的依赖性。

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摘要

Na(+) channel clustering at nodes of Ranvier in the developing rat optic nerve was analyzed to determine mechanisms of localization, including the possible requirement for glial contact in vivo. Immunofluorescence labeling for myelin-associated glycoprotein and for the protein Caspr, a component of axoglial junctions, indicated that oligodendrocytes were present, and paranodal structures formed, as early as postnatal day 7 (P7). However, the first Na(+) channel clusters were not seen until P9. Most of these were broad, and all were excluded from paranodal regions of axoglial contact. The number of detected Na(+) channel clusters increased rapidly from P12 to P22. During this same period, conduction velocity increased sharply, and Na(+) channel clusters became much more focal. To test further whether oligodendrocyte contact directly influences Na(+) channel distributions, nodes of Ranvier in the hypomyelinating mouse Shiverer were examined. This mutant has oligodendrocyte-ensheathed axons but lacks compact myelin and normal axoglial junctions. During development Na(+) channel clusters in Shiverer mice were reduced in numbers and were in aberrant locations. The subcellular location of Caspr was disrupted, and nerve conduction properties remained immature. These results indicate that in vivo, Na(+) channel clustering at nodes depends not only on the presence of oligodendrocytes but also on specific axoglial contact at paranodal junctions. In rats, ankyrin-3/G, a cytoskeletal protein implicated in Na(+) channel clustering, was detected before Na(+) channel immunoreactivity but extended into paranodes in non-nodal distributions. In Shiverer, ankyrin-3/G labeling was abnormal, suggesting that its localization also depends on axoglial contact.
机译：Na（+）通道聚集在发育中的大鼠视神经中Ranvier的节点上，以确定位置的机制，包括体内胶质接触的可能要求。髓磷脂相关糖蛋白和蛋白Caspr（一种轴突连接的组成部分）的免疫荧光标记表明，早在产后第7天（P7）就存在少突胶质细胞，并形成了淋巴结结构。但是，直到P9才看到第一个Na（+）通道簇。这些大多数是宽阔的，并且都被排除在腋窝旁淋巴结区域之外。从P12到P22，检测到的Na（+）通道簇的数量迅速增加。在同一时期，传导速度急剧增加，Na（+）通道簇变得更加集中。若要进一步测试是否少突胶质细胞接触直接影响Na（+）通道分布，检查了髓鞘发育不足的小鼠Shiverer中Ranvier的结节。该突变体具有少突胶质细胞增生的轴突，但缺乏致密的髓磷脂和正常的轴突连接。在开发过程中，Shiverer小鼠中的Na（+）通道簇数量减少并且处在异常位置。 Caspr的亚细胞位置被破坏，神经传导特性仍然不成熟。这些结果表明，在体内，节点上的Na（+）通道簇不仅取决于少突胶质细胞的存在，而且还取决于结节旁连接处的特定轴突接触。在大鼠中，锚蛋白3 / G，一种与Na（+）通道簇有关的细胞骨架蛋白，在Na（+）通道免疫反应之前被检测到，但以非节段分布扩展到节旁。在Shiverer中，锚蛋白3 / G标记异常，这表明其定位还取决于轴突接触。

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