Rothman Sarah M, Kreider Rob A, Winkelstein Beth A
Department of Bioengineering, University of Pennsylvania, Philadelphia, Pennsylvania 19104-6392, USA.
Spine (Phila Pa 1976). 2005 Nov 15;30(22):2491-6. doi: 10.1097/01.brs.0000186316.38111.4b.
Behavioral and immunohistochemical analysis in rat models of persistent and transient allodynia.
To examine separate cervical nerve root injuries (compression, transection) for producing behavioral hypersensitivity and investigate spinal neuropeptides to understand relationships to pain symptoms.
Mechanical cervical nerve root injury can be a source of neck pain. Painful lumbar radiculopathy models show that different nerve root ligation intensities produce differential allodynia responses. Spinal neuropeptides can mediate pain responses. Yet, little is known about their contributions to pain in the cervical spine.
Rats underwent separate procedures on the right C7 nerve roots: transection (n = 12), 10-gf compression for 15 minutes (n = 11), or sham (n = 5). Ipsilateral forepaw mechanical allodynia was measured after surgery for 7 days. C7 spinal cord tissue was analyzed by immunohistochemistry for substance P and calcitonin gene-related peptide (CGRP) expression on days 1 and 7 for each injury; densitometry quantified immunoreactivity in lamina I of the ipsilateral dorsal horn.
Both injuries immediately produced significant increases in allodynia. Sensitivity was sustained following root compression, and at day 7, was not different from day 1. By day 7 after transection, allodynia had returned to baseline and sham levels, significantly decreasing from day 1 (P = 0.0012). Spinal substance P and CGRP were increased over normal at day 1 for both injuries and decreased with time for CGRP after transection, which paralleled behaviors. For individual rats, substance P was significantly (P < 0.001) correlated with CGRP expression for both injuries.
Compression and transection of the cervical nerve root produce different forepaw allodynia responses, with persistent and transient sensitivity, respectively. Spinal neuropeptide expression in these models parallels this sensitivity, suggesting their potential role in pain symptoms.
持续性和短暂性异常性疼痛大鼠模型的行为学和免疫组织化学分析。
检查单独的颈神经根损伤（压迫、横断）以产生行为超敏反应，并研究脊髓神经肽以了解其与疼痛症状的关系。
机械性颈神经根损伤可能是颈部疼痛的一个来源。疼痛性腰椎神经根病模型表明，不同的神经根结扎强度会产生不同的异常性疼痛反应。脊髓神经肽可介导疼痛反应。然而，关于它们在颈椎疼痛中的作用知之甚少。
对大鼠右侧C7神经根进行单独手术：横断（n = 12）、10克力压迫15分钟（n = 11）或假手术（n = 5）。术后7天测量同侧前爪机械性异常性疼痛。对每种损伤在第1天和第7天通过免疫组织化学分析C7脊髓组织中P物质和降钙素基因相关肽（CGRP）的表达；密度测定法定量同侧背角I层的免疫反应性。
两种损伤均立即导致异常性疼痛显著增加。神经根压迫后敏感性持续存在，在第7天与第1天无差异。横断后第7天，异常性疼痛已恢复到基线和假手术水平，与第1天相比显著降低（P = 0.0012）。两种损伤在第1天脊髓P物质和CGRP均高于正常水平，横断后CGRP随时间下降，这与行为变化平行。对于个体大鼠，两种损伤的P物质与CGRP表达均显著相关（P < 0.001）。
颈神经根的压迫和横断分别产生不同的前爪异常性疼痛反应，分别为持续性和短暂性敏感性。这些模型中脊髓神经肽的表达与这种敏感性平行，表明它们在疼痛症状中可能发挥的作用。
