England J D, Gamboni F, Ferguson M A, Levinson S R
Department of Neurology, Louisiana State University School of Medicine, New Orleans 70112-2822.
Muscle Nerve. 1994 Jun;17(6):593-8. doi: 10.1002/mus.880170605.
The axolemmal distribution of voltage-gated sodium channels largely determines the regions of axonal electrical excitability. Using a well-characterized anti-sodium channel antibody, we examined peripheral nerve fibers focally injured by exposure to the neurotoxic agent, potassium tellurite (K2TeO3). Immunocytochemical and radioimmunoassay data showed a focal accumulation of sodium channels within the tips of injured axons. The major increase in sodium channel concentration occurred between 7 and 11 days after toxin exposure; however, immunocytochemically, excess sodium channels persisted in several axonal endings for a much longer time. The accumulation of sodium channels at injured axonal tips may be responsible, in part, for ectopic axonal excitability and the resulting abnormal sensory phenomena (especially pain and paresthesias) which frequently complicate peripheral nerve injury in humans.
电压门控钠通道在轴膜上的分布很大程度上决定了轴突电兴奋性的区域。我们使用一种特性明确的抗钠通道抗体，检查了因暴露于神经毒剂亚碲酸钾（K2TeO3）而受到局部损伤的周围神经纤维。免疫细胞化学和放射免疫分析数据显示，损伤轴突末端内钠通道有局部聚集。钠通道浓度的主要增加发生在毒素暴露后7至11天之间；然而，免疫细胞化学显示，多余的钠通道在几个轴突末梢中持续存在的时间要长得多。损伤轴突末端钠通道的聚集可能部分导致了异位轴突兴奋性以及由此产生的异常感觉现象（尤其是疼痛和感觉异常），这些现象常常使人类周围神经损伤变得复杂。
