Peripheral nerve injuries caused by focal constriction are characterised by local nerve ischaemia, axonal degeneration, demyelination, and neuroinflammation. The aim of this study was to understand temporal changes in the excitability properties of injured motor axons in a mouse model of nerve constriction injury (NCI). The excitability of motor axons following unilateral sciatic NCI was studied in male C57BL/6J mice distal to the site of injury at the acute (6 hours‐1 week) and chronic (up to 20 weeks) phases of injury, using threshold tracking. Multiple measures of nerve excitability, including strength‐duration properties, threshold electrotonus, current‐threshold relationship, and recovery cycle were examined using the automated nerve excitability protocol (TRONDNF). Acutely, injured motor axons developed a pattern of excitability characteristic of ischemic depolarisation. In most cases, the sciatic nerve became transiently inexcitable. When a liminal compound muscle action potential could again be recorded, it had an increase in threshold and latency, compared to both pre‐injury baseline and sham‐injured groups. These axons showed a greater threshold change in response to hyperpolarising threshold electrotonus and a significant upward shift in the recovery cycle. Mathematical modelling suggested that the changes seen in chronically injured axons involve shortened internodes, reduced myelination, and exposed juxtaparanodal fast K⁺ conductances. The findings of this study demonstrate long‐term changes in motor excitability following NCI (involving alterations in axonal properties and ion channel activity) and are important for understanding the mechanisms of neurapraxic injuries and traumatic mononeuropathies.

中文翻译：

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神经收缩损伤小鼠模型运动轴突兴奋性的电生理研究

局灶性收缩引起的周围神经损伤的特征是局部神经缺血、轴索变性、脱髓鞘和神经炎症。本研究的目的是了解神经收缩损伤 (NCI) 小鼠模型中受伤运动轴突的兴奋性随时间的变化。使用阈值跟踪，在急性（6 小时-1 周）和慢性（最多 20 周）阶段损伤部位远端的雄性 C57BL/6J 小鼠中研究了单侧坐骨神经性 NCI 后运动轴突的兴奋性。使用自动神经兴奋性协议 (TRONDNF) 检查神经兴奋性的多项测量，包括强度-持续时间特性、阈值电紧张、电流-阈值关系和恢复周期。敏锐地，受伤的运动轴突产生了缺血性去极化的兴奋性特征。在大多数情况下，坐骨神经会暂时变得麻木。当可以再次记录阈限复合肌肉动作电位时，与损伤前基线和假损伤组相比，阈值和潜伏期增加。这些轴突显示出更大的阈值变化，以响应超极化阈值电紧张和恢复周期的显着向上移动。数学模型表明，在慢性损伤的轴突中观察到的变化包括节间缩短、髓鞘形成减少和暴露的近旁快 K 与损伤前基线和假损伤组相比，它的阈值和潜伏期都有所增加。这些轴突显示出更大的阈值变化，以响应超极化阈值电紧张和恢复周期的显着向上移动。数学模型表明，在慢性损伤的轴突中观察到的变化包括节间缩短、髓鞘形成减少和暴露的近旁快 K 与损伤前基线和假损伤组相比，它的阈值和潜伏期都有所增加。这些轴突显示出更大的阈值变化，以响应超极化阈值电紧张和恢复周期的显着向上移动。数学模型表明，在慢性损伤的轴突中观察到的变化包括节间缩短、髓鞘形成减少和暴露的近旁快 K⁺电导。这项研究的结果证明了 NCI 后运动兴奋性的长期变化（涉及轴突特性和离子通道活性的改变），并且对于理解神经过度损伤和外伤性单神经病的机制很重要。