Mechanical hyperalgesia after an L5 spinal nerve lesion in the rat is not dependent on input from injured nerve fibers
Mechanical hyperalgesia after an L5 spinal nerve lesion in the rat is not dependent on input from injured nerve fibers
复制标题
DOI：
10.1016/s0304-3959(00)00250-5
复制
发表时间：
2000-04-01
期刊：
影响因子：
7.4
通讯作者：
Belzberg, AJ
中科院分区：
文献类型：
--
作者：
Li, YB;Dorsi, MJ;Belzberg, AJ
动物周围神经的损伤通常会导致神经病理性疼痛的迹象，包括对热、冷和机械刺激的痛敏。在L5脊神经结扎切断(改良SNL损毁)的大鼠中，评估了损伤的和完整的神经纤维在机械性痛敏中的作用。为了评估损伤的传入神经的贡献，在改良的SNL损伤前立即或之后7天进行L5背根切断术。为了研究邻近完整脊神经的作用，在改良的SNL损伤后7天进行了L4背根切断术。用Dixon的升降法(Dixon WJ，Annu Rev Pharmacol Toxicol 1980；20：441-462)在大鼠后掌对应的L3、L4和L5皮肤体的三个部位测量机械刺激的缩爪阈值。我们发现，改良的SNL损毁产生了显著的、持续的(20天)机械性戒断阈值降低。机械性痛觉过敏的严重程度和持续时间因测试地点而异。L5和JA皮肤刀测试部位出现了最严重和最持久的机械性痛敏。相比之下，L3测试部位发生的机械性痛敏明显不那么严重，持续时间也更短。L5背根切断本身可引起机械抽离阈值的一过性下降。在改良的SNL损毁前或后7天行L5背根切断术并不能阻止或解决观察到的机械戒断阈值的降低。在改良的SNL损伤后7天行L4背根切断术，导致机械撤退阈值立即恢复到基线值。这些结果表明，在L5脊神经结扎和切断后，机械性痛敏的发展和持续不依赖于受损传入的输入。我们认为，神经损伤后发展的沃勒变性导致了受损脊神经的退变纤维与相邻脊神经的完整纤维之间的相互作用。这导致了完整纤维的变化，这些纤维对机械性痛觉过敏的启动和维持都起着关键作用。(C)2000年国际疼痛研究协会。爱思唯尔科学公司出版。版权所有。
An injury to a peripheral nerve in animals often leads to signs of neuropathic pain including hyperalgesia to heat, cold and mechanical stimuli. The role of injured and intact nerve fibers in mechanical hyperalgesia was evaluated in rats subjected to an L5 spinal nerve ligation-and-cut ('modified SNL lesion'). To assess the contribution of injured afferents, an L5 dorsal rhizotomy was performed immediately before, or 7 days after the modified SNL lesion. To study the role of adjacent intact spinal nerves, an L4 dorsal rhizotomy was performed 7 days after the modified SNL lesion. The up-down method of Dixon (Dixon WJ, Annu Rev Pharmacol Toxicol 1980;20:441-462) was used to measure the paw withdrawal threshold to mechanical stimuli at three sites on the rat hindpaw corresponding to the L3, L4, and L5 dermatomes. We found that the modified SNL lesion produced a significant, lasting (>20 days) decrease of the mechanical withdrawal threshold. The severity and duration of mechanical hyperalgesia varied across testing sites. The L5 and JA dermatome test sites developed the most severe and lasting mechanical hyperalgesia. In contrast, the L3 testing site developed significantly less severe and shorter lasting mechanical hyperalgesia. L5 dorsal rhizotomy, by itself, produced a transient decrease in mechanical withdrawal thresholds. L5 dorsal rhizotomy performed before, or 7 days after, the modified SNL lesion did not prevent or resolve the observed decrease in mechanical withdrawal thresholds. L4 dorsal rhizotomy performed 7 days after the modified SNL lesion resulted in an immediate reversal of mechanical withdrawal thresholds back to baseline values. These results suggest that, after L5 spinal nerve ligation-and-cut, mechanical hyperalgesia develops and persists independent of input from injured afferents. We propose that the Wallerian degeneration that develops after a nerve injury leads to interactions between the degenerating fibers of the injured spinal nerve and the intact fibers of adjacent spinal nerves. This leads to changes in the intact fibers that play a critical role for both initiation and maintenance of mechanical hyperalgesia. (C) 2000 International Association for the Study of Pain. Published by Elsevier Science B.V. All rights reserved.