Time course of ongoing activity during neuritis and following axonal transport disruption.
Time course of ongoing activity during neuritis and following axonal transport disruption.
复制标题
神经炎期间和轴突运输中断后持续活动的时间过程。
DOI：
10.1152/jn.00882.2017
复制
发表时间：
2018
影响因子：
2.5
通讯作者：
Dilley,Andrew
中科院分区：
文献类型：
--
作者：
Satkeviciute,Ieva;Goodwin,George;Bove,GeoffreyM;Dilley,Andrew
局部神经炎症（神经炎）导致沿完整伤害感受器轴突的持续活动和轴突机械敏感性（AMS），并破坏轴突运输。这种现象形成了放射性疼痛最可能的原因，如坐骨神经痛。我们之前的研究表明，没有炎症或变性的轴突运输中断也会导致AMS，但在AMS发生时，尽管会引起皮肤过敏，但不会引起持续的活动。然而，在神经炎或非炎症性轴突运输中断期间，尚无系统的活动研究。在这项研究中，我们展示了神经炎和长春花碱诱导的轴突运输中断后初级感觉神经元持续活动的时间过程。尽管24%的C/慢速A-纤维神经元在神经炎期间持续活动，但在长春花碱治疗后1-15天，很少（<10%）的A-和C-纤维神经元显示持续活动。相比之下，AMS在长春花碱处理部位短暂增加，在第4-5天达到峰值（28%的C/慢a -纤维神经元），并在第15天消退。各组传导速度均减慢。综上所述，无炎症的轴突运输中断不会导致感觉神经元（包括伤害感受器）的持续活动，但确实会导致AMS的快速和短暂发展。由于有人提出AMS是机械诱发放射性疼痛的基础，而轴突运输的短暂中断（如先前报道）导致短暂性AMS，因此，破坏轴突运输的过程，如神经炎，必须持续存在以维持AMS和相关症状。许多放射性疼痛患者在临床检查中没有神经损伤的迹象，但可能有神经炎，这破坏了轴突运输。我们已经证明，轴突运输中断不会诱导初级感觉神经元的持续活动，但确实会引起短暂的轴突机械敏感性。目前的数据完成了轴突运输中断后关键轴突敏感性的概况。总的来说，这种情况支持活跃的外周过程是维持轴突敏感性所必需的。
Local nerve inflammation (neuritis) leads to ongoing activity and axonal mechanical sensitivity (AMS) along intact nociceptor axons and disrupts axonal transport. This phenomenon forms the most feasible cause of radiating pain, such as sciatica. We have previously shown that axonal transport disruption without inflammation or degeneration also leads to AMS but does not cause ongoing activity at the time point when AMS occurs, despite causing cutaneous hypersensitivity. However, there have been no systematic studies of ongoing activity during neuritis or noninflammatory axonal transport disruption. In this study, we present the time course of ongoing activity from primary sensory neurons following neuritis and vinblastine-induced axonal transport disruption. Whereas 24% of C/slow Aδ-fiber neurons had ongoing activity during neuritis, few (<10%) A- and C-fiber neurons showed ongoing activity 1–15 days following vinblastine treatment. In contrast, AMS increased transiently at the vinblastine treatment site, peaking ondays 4–5(28% of C/slow Aδ-fiber neurons) and resolved byday 15. Conduction velocities were slowed in all groups. In summary, the disruption of axonal transport without inflammation does not lead to ongoing activity in sensory neurons, including nociceptors, but does cause a rapid and transient development of AMS. Because it is proposed that AMS underlies mechanically induced radiating pain, and a transient disruption of axonal transport (as previously reported) leads to transient AMS, it follows that processes that disrupt axonal transport, such as neuritis, must persist to maintain AMS and the associated symptoms.NEW & NOTEWORTHYMany patients with radiating pain lack signs of nerve injury on clinical examination but may have neuritis, which disrupts axonal transport. We have shown that axonal transport disruption does not induce ongoing activity in primary sensory neurons but does cause transient axonal mechanical sensitivity. The present data complete a profile of key axonal sensitivities following axonal transport disruption. Collectively, this profile supports that an active peripheral process is necessary for maintained axonal sensitivities.