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大鼠神经根施加髓核后背根神经节神经元中酸敏感离子通道3的上调

Up-regulation of acid-sensing ion channel 3 in dorsal root ganglion neurons following application of nucleus pulposus on nerve root in rats.

作者信息

Ohtori Seiji, Inoue Gen, Koshi Takana, Ito Toshinori, Doya Hideo, Saito Tomoko, Moriya Hideshige, Takahashi Kazuhisa

机构信息

Department of Orthopaedic Surgery, Graduate School of Medicine, Chiba University, Chiba, Japan.

出版信息

Spine (Phila Pa 1976). 2006 Aug 15;31(18):2048-52. doi: 10.1097/01.brs.0000231756.56230.13.

Abstract

STUDY DESIGN

Immunocytochemistry for acid-sensing ion channel 3 (ASIC3) in neurons of rat dorsal root ganglions (DRGs) from animals exposed to a model of lumbar disc herniation.

OBJECTIVE

To examine expression of ASIC3 in DRGs and the effect of a sodium channel blocker applied to the nerve root in a rat model of lumbar disc herniation.

SUMMARY OF BACKGROUND DATA

Radicular pain is a common symptom of lumbar disc herniation in human beings. A depolarizing sodium channel gated by protons during tissue acidosis, ASIC3, is specifically expressed in sensory neurons. It has been associated with cardiac ischemic and inflammatory pain. We often perform spinal nerve root block for radicular pain using a sodium channel blocker, such as lidocaine; however, it has been unclear whether the effective period of this treatment is usually longer than the expected duration of efficacy.

METHODS

For the lumbar disc herniation model, nucleus pulposus was harvested from the tail and applied to the L5 nerve root, and the nerve roots were pinched. We evaluated mechanical allodynia in sham-operated animals and a disc herniation model. Immunohistochemistry was used to examine ASIC3 expression in L5 DRGs. Finally, the effect of lidocaine on pain and ASIC3 expression in the disc herniation model was examined.

RESULTS

Animals exposed to the lumbar disc herniation model showed allodynia for 8 days, and ASIC3 immunoreactivity was up-regulated in DRG neurons. After administration of lidocaine to spinal nerve roots affected by disc herniation, ASIC3 immunoreactivity was down-regulated in DRG neurons, and the level of mechanical allodynia was significantly decreased for 8 days.

CONCLUSIONS

Our results suggest that ASIC3 in DRG neurons may play an important role in nerve root pain caused by lumbar disc herniation. Lidocaine decreased ASIC3 expression in DRG neurons and pain associated with the disc herniation model.

摘要

研究设计

对暴露于腰椎间盘突出症模型的动物的大鼠背根神经节(DRG)神经元进行酸敏感离子通道3(ASIC3)的免疫细胞化学研究。

目的

研究ASIC3在DRG中的表达以及在大鼠腰椎间盘突出症模型中应用钠通道阻滞剂对神经根的影响。

背景数据总结

神经根性疼痛是人类腰椎间盘突出症的常见症状。ASIC3是一种在组织酸中毒时由质子门控的去极化钠通道,在感觉神经元中特异性表达。它与心脏缺血性疼痛和炎性疼痛有关。我们经常使用钠通道阻滞剂(如利多卡因)对神经根性疼痛进行脊神经根阻滞;然而,这种治疗的有效期限是否通常长于预期疗效持续时间尚不清楚。

方法

对于腰椎间盘突出症模型,从尾部采集髓核并应用于L5神经根,然后对神经根进行挤压。我们评估了假手术动物和椎间盘突出症模型中的机械性异常性疼痛。采用免疫组织化学法检测L5 DRG中ASIC3的表达。最后,研究了利多卡因对椎间盘突出症模型疼痛和ASIC3表达的影响。

结果

暴露于腰椎间盘突出症模型的动物出现8天的异常性疼痛,DRG神经元中ASIC3免疫反应性上调。对受椎间盘突出影响的脊神经根给予利多卡因后,DRG神经元中ASIC3免疫反应性下调,机械性异常性疼痛水平在8天内显著降低。

结论

我们的结果表明,DRG神经元中的ASIC3可能在腰椎间盘突出症引起的神经根性疼痛中起重要作用。利多卡因降低了DRG神经元中ASIC3的表达以及与椎间盘突出症模型相关的疼痛。

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