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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >A comparison of the potential role of the tetrodotoxin-insensitive sodium channels,PN3/SNS and NaN/SNS2,in rat models of chronic pain
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A comparison of the potential role of the tetrodotoxin-insensitive sodium channels,PN3/SNS and NaN/SNS2,in rat models of chronic pain

机译：河豚毒素不敏感钠通道，PN3 / SNS和NaN / SNS2在慢性疼痛大鼠模型中的潜在作用比较

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摘要

Alterations in sodium channel expression and function have been suggested as a key molecular event underlying the abnormal processing of pain after peripheral nerve or tissue injury. Although the relative contribution of individual sodium channel subtypes to this process is unclear, the biophysical properties of the tetrodotoxin-resistant current, mediated, at least in part ,by the sodium channel PN3 (SNS),suggests that it may play a specialized, pathophysiological role in the sustained, repetitive firing of the peripheral neuron after injury. Moreover ,this hypothesis is supported by evidence demonstrating that selective "knock-down" of PN3 protein in the dorsal root ganglion with specific antisense oligodeoxynucleotides prevents hyperalgesia and allodynia caused by either chronic nerve or tissue injury. In contrast, knock-down of NaN/SNS2 protein, a sodium channel that may be a second possible candidate for the tetrosotoxin-resistant current ,appears to have no effect on nerve injury-induced behavioral responses. These data suggest that relief from chronic inflammatory or neuropathic pain might be achieved by selective blockade or inhibition of PN3 expression. In light of ther restricted distribution of PN3 to sensory neurons, such an approach might offer effective pain relief without a significant side-effect liability
机译：已提出钠通道表达和功能的改变是周围神经或组织损伤后疼痛异常处理的关键分子事件。尽管个别钠通道亚型对此过程的相对贡献尚不清楚，但河豚毒素抗性电流的生物物理特性至少部分地由钠通道PN3（SNS）介导，这表明它可能起专门的病理生理作用。在损伤后持续，反复激发周围神经元中起重要作用。此外，该假设得到证据的支持，该证据表明，使用特定的反义寡聚脱氧核苷酸选择性地“敲低”背根神经节中的PN3蛋白可以防止由慢性神经或组织损伤引起的痛觉过敏和异常性疼痛。相反，敲除NaN / SNS2蛋白（钠通道可能是抗河豚毒素的电流的第二个可能的候选物）似乎对神经损伤诱导的行为反应没有影响。这些数据表明，可以通过选择性阻滞或抑制PN3表达来减轻慢性炎症或神经性疼痛。鉴于PN3在感觉神经元中的分布受到限制，这种方法可能可以有效缓解疼痛，而不会产生明显的副作用

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