School of Physiology and Pharmacology, University of Bristol, Bristol BS8 1TD, UK.
Pain. 2012 Sep;153(9):1824-1836. doi: 10.1016/j.pain.2012.04.019. Epub 2012 Jun 20.
Partial nerve injury leads to peripheral neuropathic pain. This injury results in conducting/uninterrupted (also called uninjured)sensory fibres, conducting through the damaged nerve alongside axotomised/degenerating fibres. In rats seven days after L5 spinal nerve axotomy (SNA) or modified-SNA (added loose-ligation of L4 spinal nerve with neuroinflammation-inducing chromic-gut),we investigated (a) neuropathic pain behaviours and (b) electrophysiological changes in conducting/uninterrupted L4 dorsal root ganglion (DRG) neurons with receptive fields (called: L4-receptive-field-neurons). Compared to pretreatment, modified-SNA rats showed highly significant increases in spontaneous-foot lifting duration, mechanical-hypersensitivity/allodynia, and heathypersensitivity/hyperalgesia, that were significantly greater than after SNA, especially spontaneous-foot-lifting. We recorded intracellularly in vivo from normal L4/L5 DRG neurons and ipsilateral L4-receptive-field-neurons. After SNA or modified-SNA, L4-receptive-field-neurons showed the following: (a) increased percentages of C-, Aδ-, and Aβ-nociceptors and cutaneous Aα/β-low-thresholdmechanoreceptors with ongoing/spontaneous firing; (b) spontaneous firing in C-nociceptors that originated peripherally; this was ata faster rate in modified-SNA than SNA; (c) decreased electricalthresholds in A-nociceptors after SNA; (d) hyperpolarised membrane potentials in A-nociceptors and Aα/-low-thresholdmechanoreceptors after SNA, but not C-nociceptors; (e) decreased somatic action potential rise times in C- and A-nociceptors, not Aα/β-low-threshold-mechanoreceptors. We suggest that these changes in subtypes of conducting/uninterrupted neurons after partial nerve injury contribute to the different aspects of neuropathic pain as follows: spontaneous firing in nociceptors to ongoing/spontaneous pain; spontaneous firing in Aα/β-low-threshold-mechanoreceptors to dysesthesias/paresthesias; and lowered A-nociceptor electrical thresholds to A-nociceptor sensitization,and greater evoked pain [corrected].
部分神经损伤导致周围神经性疼痛。这种损伤导致传导/未中断（也称为未损伤）感觉纤维与轴突切断/退化纤维一起通过受损的神经传导。在 L5 脊髓神经切断术（SNA）或改良 SNA（在 L4 脊髓神经上增加松散结扎引起神经炎症的铬肠）后 7 天的大鼠中，我们研究了（a）神经性疼痛行为和（b）传导/未中断 L4 背根神经节（DRG）神经元的电生理变化，这些神经元具有感受野（称为：L4 感受野神经元）。与预处理相比，改良 SNA 大鼠的自发性抬脚持续时间、机械性超敏反应/痛觉过敏和热敏反应/痛觉过敏显著增加，显著高于 SNA 后，特别是自发性抬脚。我们在体内从正常的 L4/L5 DRG 神经元和同侧的 L4 感受野神经元进行了记录。在 SNA 或改良 SNA 后，L4 感受野神经元表现出以下特征：（a）增加 C-、Aδ-和 Aβ-伤害感受器以及持续/自发性放电的皮肤 Aα/β-低阈值机械感受器的百分比；（b）起源于外周的 C-伤害感受器的自发性放电，在改良 SNA 中比 SNA 更快；（c）SNA 后 A-伤害感受器的电阈值降低；（d）SNA 后 A-伤害感受器和 Aα/-低阈值机械感受器的膜电位超极化，但 C-伤害感受器没有；（e）C-和 A-伤害感受器的体感觉动作电位上升时间缩短，Aα/β-低阈值机械感受器没有。我们认为，部分神经损伤后传导/未中断神经元的这些亚型变化有助于神经性疼痛的不同方面，如下所示：伤害感受器的自发性放电与持续性/自发性疼痛有关；Aα/β-低阈值机械感受器的自发性放电与感觉异常/感觉异常有关；A-伤害感受器的电阈值降低与 A-伤害感受器的敏化有关，并且引起更大的诱发疼痛[校正]。
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