Up-regulation of acid-sensing ion channel 3 in dorsal root ganglion neurons following application of nucleus pulposus on nerve root in rats
Up-regulation of acid-sensing ion channel 3 in dorsal root ganglion neurons following application of nucleus pulposus on nerve root in rats
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DOI：
10.1097/01.brs.0000231756.56230.13
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发表时间：
2006-08-15
期刊：
影响因子：
3
通讯作者：
Takahashi, Kazuhisa
中科院分区：
文献类型：
--
作者：
Ohtori, Seiji;Inoue, Gen;Takahashi, Kazuhisa
研究设计。腰椎间盘突出症大鼠背根神经节（DRGs）神经元酸感离子通道3 （ASIC3）的免疫细胞化学研究目的观察大鼠腰椎间盘突出症DRGs中ASIC3的表达及钠通道阻滞剂对神经根的影响。背景资料摘要。神经根性疼痛是腰椎间盘突出症的常见症状。组织酸中毒过程中质子门控的去极化钠通道ASIC3在感觉神经元中特异性表达。它与心脏缺血性和炎症性疼痛有关。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，目前尚不清楚这种治疗的有效时间是否通常比预期的有效时间更长。对于腰椎间盘突出模型，从尾部取髓核，施加于L5神经根，捏紧神经根。我们在假手术动物和椎间盘突出模型中评估机械异常性痛。免疫组化检测L5 DRGs中ASIC3的表达。最后，观察利多卡因对腰椎间盘突出症模型疼痛及ASIC3表达的影响。暴露于腰椎间盘突出模型的动物出现8天的异常性疼痛，DRG神经元中ASIC3免疫反应性上调。利多卡因治疗腰椎间盘突出症脊髓神经根后，DRG神经元ASIC3免疫反应性下调，机械性异常痛水平明显降低，持续8 d。我们的研究结果提示DRG神经元中的ASIC3可能在腰椎间盘突出症引起的神经根疼痛中起重要作用。利多卡因降低DRG神经元中ASIC3的表达和与椎间盘突出模型相关的疼痛。
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.