Hulse R P
Cancer Biology, School of Medicine, University of Nottingham, Queen's Medical Centre, UK.
Eur J Pain. 2016 Apr;20(4):615-25. doi: 10.1002/ejp.779. Epub 2015 Oct 2.
C fibre hyperexcitability is fundamental to chronic pain development in humans and rodents; therefore, peripheral sensory neuronal sensitization plays a role in the development of mechanical hyperalgesia. However, the axonal properties and underlying mechanisms that are associated to these chronic pain states still require investigation.
Teased fibre electrophysiology of the saphenous nerve was used to identify C fibres in naïve and nerve-injured rats. C fibres were identified using electrical stimulation which further provided conduction velocity slowing profiles. From these nerve filaments evoked responses to mechanical stimuli were recorded. Vehicle or galanin were applied directly to the saphenous nerve trunk prior to stimulation.
Increased levels of mechanically evoked activity in mechano-sensitive C fibres was associated to reduced conduction failure, enhanced conduction velocity latency recovery and reduced conduction velocity slowing. Mechanical hyperalgesia developed in nerve-injured animals in which mechano-sensitive C fibres demonstrated increased mechanically evoked responses and reduced rate of adaptation. Mechano-sensitive C fibres in nerve-injured animals had reduced levels of conduction velocity slowing, enhanced rate of conduction velocity recovery and reduced firing frequency failure versus naïve animals; all hallmarks of enhanced sensory neuronal excitability. Directly applying the antinociceptive agent galanin to the saphenous nerve trunk in naive animals led to increased conduction failure, reduced latency recovery rate and increased levels of conduction velocity slowing.
Nerve injury-induced enhanced neural responses to mechanical stimulation are associated to defined parameters setout by conduction velocity slowing, mediated via axonal processing. Application of galanin inhibits axonal excitability.
C纤维的过度兴奋是人类和啮齿动物慢性疼痛发展的基础；因此，外周感觉神经元致敏在机械性痛觉过敏的发展中起作用。然而，与这些慢性疼痛状态相关的轴突特性和潜在机制仍有待研究。
采用隐神经单纤维电生理学方法，在未受伤和神经损伤的大鼠中识别C纤维。通过电刺激识别C纤维，这进一步提供了传导速度减慢的情况。从这些神经细丝记录对机械刺激的诱发反应。在刺激前，将载体或甘丙肽直接应用于隐神经干。
机械敏感C纤维中机械诱发活动水平的增加与传导失败减少、传导速度潜伏期恢复增强和传导速度减慢减少有关。在神经损伤的动物中出现了机械性痛觉过敏，其中机械敏感C纤维表现出机械诱发反应增加和适应率降低。与未受伤动物相比，神经损伤动物中的机械敏感C纤维传导速度减慢水平降低、传导速度恢复率增强且放电频率失败减少；所有这些都是感觉神经元兴奋性增强的标志。在未受伤的动物中，将抗伤害感受剂甘丙肽直接应用于隐神经干会导致传导失败增加、潜伏期恢复率降低和传导速度减慢水平增加。
神经损伤引起的对机械刺激的神经反应增强与通过轴突处理介导的传导速度减慢所设定的特定参数有关。甘丙肽的应用会抑制轴突兴奋性。
