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首页> 外文期刊>The European Journal of Neuroscience >Abnormal axonal physiology is associated with altered expression and distribution of Kv1.1 and Kv1.2 K+ channels after chronic spinal cord injury.
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Abnormal axonal physiology is associated with altered expression and distribution of Kv1.1 and Kv1.2 K+ channels after chronic spinal cord injury.

机译：慢性脊髓损伤后，轴突生理异常与Kv1.1和Kv1.2 K +通道的表达和分布改变有关。

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摘要

Dysfunction of surviving axons which traverse the site of spinal cord injury (SCI) has been linked to altered sensitivity to the K+ channel blocker 4-aminopyridine (4-AP) and appears to contribute to post-traumatic neurological deficits although the underlying mechanisms remain unclear. In this study, sucrose gap electrophysiology in isolated dorsal column strips, Western blotting and confocal immunofluorescence microscopy were used to identify the K+ channels associated with axonal dysfunction after chronic (6-8 weeks postinjury) clip compresssion SCI of the thoracic cord at T7 in rats. The K+ channel blockers 4-AP (200 microM, 1 mM and 10 mM) and alpha-dendrotoxin (alpha-DTX, 500 nM) resulted in a significant relative increase in the amplitude and area of compound action potentials (CAP) recorded from chronically injured dorsal column axons in comparison with control noninjured preparations. In contrast, TEA (10 mM) and CsCl (2 mM) had similar effects on injured and control spinal cord axons. Western blotting and quantitative immunofluorescence microscopy showed increased expression of Kv1.1 and Kv1.2 K+ channel proteins on spinal cord axons following injury. In addition, Kv1.1 and Kv1.2 showed a dispersed staining pattern along injured axons in contrast to a paired juxtaparanodal localization in uninjured spinal cord axons. Furthermore, labelled alpha-DTX colocalized with Kv1.1 and Kv1.2 along axons. These findings suggest a novel mechanism of axonal dysfunction after SCI whereby an increased 4-AP- and alpha-DTX-sensitive K+ conductance, mediated in part by increased Kv1.1 and Kv1.2 K+ channel expression, contributes to abnormal axonal physiology in surviving axons.
机译：穿越脊髓损伤（SCI）部位的存活轴突功能障碍与对K +通道阻滞剂4-氨基吡啶（4-AP）敏感性的改变有关，尽管潜在的机制尚不清楚，但似乎促成创伤后神经功能缺损。 。在这项研究中，使用蔗糖间隙电生理在孤立的背侧柱状条带中进行Western印迹和共聚焦免疫荧光显微镜检查，以鉴定大鼠在T7时慢性（损伤后6-8周）夹压缩SCI后与轴突功能障碍相关的K +通道。 。 K +通道阻滞剂4-AP（200 microM，1 mM和10 mM）和α-树突毒素（alpha-DTX，500 nM）导致长期记录的复合动作电位（CAP）的幅度和面积显着相对增加与对照的未损伤制剂相比，背柱轴突受伤。相反，TEA（10 mM）和CsCl（2 mM）对受伤和控制的脊髓轴突具有相似的作用。 Western印迹和定量免疫荧光显微镜检查显示，损伤后脊髓轴突上Kv1.1和Kv1.2 K +通道蛋白的表达增加。此外，Kv1.1和Kv1.2在受伤的轴突上显示出分散的染色模式，这与未损伤的脊髓轴突中成对的近伞状旁突定位有关。此外，标记的α-DTX与Kv1.1和Kv1.2沿着轴突共定位。这些发现表明SCI后轴突功能障碍的新机制，其中部分由增加的Kv1.1和Kv1.2 K +通道表达介导的4-AP-和α-DTX敏感的K +电导增加，有助于存活的轴突生理异常。轴突。

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