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首页> 外文期刊>The European Journal of Neuroscience >Temporal and spatial patterns of Kv1.1 and Kv1.2 protein and gene expression in spinal cord white matter after acute and chronic spinal cord injury in rats: implications for axonal pathophysiology after neurotrauma.
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Temporal and spatial patterns of Kv1.1 and Kv1.2 protein and gene expression in spinal cord white matter after acute and chronic spinal cord injury in rats: implications for axonal pathophysiology after neurotrauma.

机译：大鼠急性和慢性脊髓损伤后脊髓白质中Kv1.1和Kv1.2蛋白的时空分布和基因表达：对神经外伤后轴突病理生理学的影响。

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摘要

After spinal cord injury (SCI), surviving white matter axons display axonal dysfunction associated with demyelination and altered K+ channel activity. To clarify the molecular basis of posttraumatic axonal pathophysiology after SCI, we investigated the changes in expression and distribution of the axonal K+ channel subunits Kv1.1 and Kv1.2 in spinal cord white matter after in vivo SCI in the rat. Using Western blot analysis, we found an increased expression of Kv1.1 and Kv1.2 at 2 and 6 weeks after SCI. By real-time PCR we observed an increase in Kv1.1 and Kv1.2 mRNA levels 1 day after SCI, which persisted until 6 weeks. Confocal immunohistochemistry showed a markedly dispersed labelling of Kv1.1 and Kv1.2 along the injured axons, in contrast to the tight localization of these channels to the juxtaparanodes of noninjured axons. This redistribution of Kv1.1 and Kv1.2 occurred as early as 1 h postinjury along some injured axons, and persisted at 6 weeks postinjury. In parallel with the redistribution of Kv1.1 and 1.2, contactin-associated protein (Caspr), which is normally confined to a paranodal location, also displayed a more diffuse distribution along the injured spinal cord axons. Our results suggest that the increased expression of Kv1.1 and Kv1.2 proteins is transcriptionally regulated. In contrast, the redistribution of the axonal K+ channel subunits occurs very early postinjury and probably reflects a disruption of the juxtaparanodal axonal region due to physical trauma, as shown by altered localization of Caspr.
机译：脊髓损伤（SCI）后，幸存的白质轴突显示出与脱髓鞘和改变的K +通道活性有关的轴突功能障碍。为了阐明脊髓损伤后创伤后轴突病理生理学的分子基础，我们研究了大鼠体内脊髓损伤后脊髓白质中轴突K +通道亚基Kv1.1和Kv1.2表达和分布的变化。使用蛋白质印迹分析，我们发现SCI后2周和6周时Kv1.1和Kv1.2的表达增加。通过实时PCR，我们观察到SCI后1天Kv1.1和Kv1.2 mRNA水平增加，并持续到6周。共聚焦免疫组织化学显示沿损伤轴突的Kv1.1和Kv1.2标记明显分散，这与这些通道紧密定位于未损伤轴突的近节相似。 Kv1.1和Kv1.2的这种重新分配最早在受伤后1小时沿一些受伤的轴突发生，并在受伤后6周持续存在。与Kv1.1和1.2的重新分布并行的是，接触蛋白相关蛋白（Caspr）通常局限在淋巴结旁，也沿受伤的脊髓轴突显示出更分散的分布。我们的结果表明，Kv1.1和Kv1.2蛋白表达的增加受到转录调控。相比之下，轴突K +通道亚基的重新分布在受伤后很早就发生了，并且可能反映了由于物理创伤导致的近伞旁结轴突区的破坏，如Caspr的局部位置改变所示。

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