The role of graded nerve root compression on axonal damage, neuropeptide changes, and pain-related behaviors.

The role of graded nerve root compression on axonal damage, neuropeptide changes, and pain-related behaviors.
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DOI:
10.4271/2008-22-0002
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发表时间:
2008-11
影响因子:
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通讯作者:
R. D. Hubbard;K. Quinn;J. J. Martínez-J.;B. Winkelstein
R. D. Hubbard;K. Quinn;J. J. Martínez-J.;B. Winkelstein
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文献类型:
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作者:
R. D. Hubbard;K. Quinn;J. J. Martínez-J.;B. Winkelstein

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颈部快速运动会对颈神经根造成负荷并产生持续性疼痛。这项研究调查了根性疼痛的细胞基础和组织负荷率的机械影响。在背根压缩的体内大鼠模型中施加一定范围的峰值负荷,并测量机械异常性疼痛(即疼痛)。在损伤后第 1 天和第 7 天,对不同组大鼠受压背根的轴突和细胞体中的轴突损伤和伤害性介质进行评估。在第 7 天的组中,通过重链神经丝免疫反应性下降来评估,压缩轴突的损伤在超过 34.08 mN 的负荷时会增加,这与该模型中产生持续性疼痛的负荷阈值相似。此外,随着背根神经节小伤害性神经元负荷的增加,神经肽物质 P 和胶质细胞系源性神经营养因子及其受体显着减少 (p < 0.02),这表明轴突损伤也可能减少受伤的伤害性传入纤维中的神经营养支持。在另一项研究中,根部以 2 毫米/秒的速度压缩并保持,以开发准线性粘弹性模型,该模型通过与准静态载荷的比较进行验证。该模型表明,与准静态速率相比,动态加载过程中达到轴突损伤载荷阈值所需的位移减少了近 23%。总之,这些研究表明,产生疼痛症状的神经根压迫足以介导伤害性细胞变化,并且对于动态负载情况,疼痛和伤害性病理生理学的阈值可能较低。
Rapid neck motions can load cervical nerve roots and produce persistent pain. This study investigated the cellular basis of radicular pain and mechanical implications of tissue loading rate. A range of peak loads was applied in an in vivo rat model of dorsal root compression, and mechanical allodynia (i.e. pain) was measured. Axonal damage and nociceptive mediators were assessed in the axons and cell bodies of compressed dorsal roots in separate groups of rats at days 1 and 7 after injury. In the day 7 group, damage in the compressed axons, evaluated by decreased heavy chain neurofilament immunoreactivity, was increased for compressions above a load of 34.08 mN, which is similar to the load-threshold for producing persistent pain in that model. Also, the neuropeptide substance P and glial cell line-derived neurotrophic factor and its receptor significantly decreased (p < 0.02) with increasing load in the small nociceptive neurons of the dorsal root ganglion, suggesting that axonal damage may also decrease neurotrophic support in injured nociceptive afferent fibers. In a separate study, roots were compressed at 2mm/s, and held, to develop a quasi-linear viscoelastic model that was validated through comparisons to quasistatic loading. The model demonstrated that nearly 23% less displacement was required to reach the axonal injury load threshold during dynamic loading than for quasistatic rates. Together, these studies demonstrate that nerve root compressions that produce pain symptoms are sufficient to mediate nociceptive cellular changes, and that thresholds for pain and nociceptive pathophysiology may be lower for dynamic loading scenarios.