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首页> 外文期刊>Brain research >Redistribution of voltage-gated sodium channels after nerve decompression contributes to relieve neuropathic pain in chronic constriction injury
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Redistribution of voltage-gated sodium channels after nerve decompression contributes to relieve neuropathic pain in chronic constriction injury

机译：神经减压后电压门控钠通道的重新分布有助于缓解慢性压迫性损伤的神经性疼痛

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Nerve decompression is an important therapeutic strategy to relieve neuropathic pain and promote the peripheral nerve regeneration. To address these issues, we investigated the effects of nerve decompression on relief of neuropathic pain behaviors, redistribution of voltage-gated sodium channels (VGSCs), and skin reinnervation with chronic constriction injury (CCI). At post-operative week (POW) 4, animals were divided into a decompression group, in which the ligatures were removed, and a CCI group, in which the ligatures remained. Thermal hyperalgesia and mechanical allodynia at POW 8 had distinct reductions in decompression group compared to CCI group. At that time in CCI group, morphological evidence of pan VGSCs (Pan Nav) and isoforms of VGSCs (Nav1.6, Nav1.9, except for Nav1.8) were shown the widely distribution along the injured sciatic nerve. All of the VGSCs in decompression group became clustering around the node of Ranvier, similar to the pattern of control sciatic nerve at POW 8. Skin reinnervation was demonstrated by epidermal nerve density (END) for protein gene product 9.5 (PGP 9.5)-immunoreactive (IR) nerve fibers and a significant difference between groups only at POW 24 (p=0.01). Growth-associated protein 43 (GAP-43) is participated in the nerve fiber growth and sprouting, a difference in END for GAP-43-IR nerve fibers at POW 24 between groups were also significant (p=0.02). These observations demonstrated that nerve decompression was accompanied with the disappearance of neuropathic pain behaviors after CCI. Morphological studies provided the evidence that redistribution of VGSCs along the injured sciatic nerve but still with an incomplete skin reinnervation. These significant findings demonstrated a role of VGSCs in the pathogenesis of neuropathic pain, and gave an approaching in pharmacological basis of therapeutics.
机译：神经减压是缓解神经性疼痛并促进周围神经再生的重要治疗策略。为了解决这些问题，我们研究了神经减压对缓解神经性疼痛行为，电压门控钠通道（VGSC）的重新分布以及慢性收缩性损伤（CCI）引起的皮肤神经支配的影响。术后第4周（POW），将动物分为减压组（其中去除了结扎）和CCI组（其中保留了结扎）。与CCI组相比，POW 8组的热痛觉过敏和机械性异常性疼痛的减压组明显减少。当时，在CCI组中，泛VGSCs（Pan Nav）和VGSCs亚型（Nav1.6，Nav1.9，除了Nav1.8）的形态学证据显示沿受损的坐骨神经广泛分布。减压组中的所有VGSC都聚集在Ranvier结周围，类似于POW 8上的坐骨神经对照模式。蛋白基因产物9.5（PGP 9.5）-免疫反应性（表皮神经密度（END）证明了皮肤的神经支配）。 IR）神经纤维和组之间的显着差异仅在POW 24（p = 0.01）。生长相关蛋白43（GAP-43）参与神经纤维的生长和发芽，两组之间在POW 24处GAP-43-IR神经纤维的END差异也很显着（p = 0.02）。这些观察结果表明，CCI后神经减压伴随着神经性疼痛行为的消失。形态学研究提供了证据，表明VGSCs沿着受损的坐骨神经重新分布，但皮肤神经支配不完全。这些重要发现证明了VGSC在神经性疼痛发病机理中的作用，并为治疗方法的药理学基础提供了一种途径。

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