An experimental model for chronic compression of dorsal root ganglion produced by intervertebral foramen stenosis in the rat
An experimental model for chronic compression of dorsal root ganglion produced by intervertebral foramen stenosis in the rat
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DOI：
10.1016/s0304-3959(98)00067-0
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发表时间：
1998-07-01
期刊：
影响因子：
7.4
通讯作者：
Xing, JL
中科院分区：
文献类型：
--
作者：
Hu, SJ;Xing, JL
在麻醉和无菌手术下，将一根小的不锈钢棒（长4 mm，直径0.5- 0.8mm）插入大鼠L5椎间孔中，形成椎间孔狭窄，从而产生背根神经节（DRG）的慢性稳定压迫。损伤侧的后爪表现出对有害热的足缩回潜伏期的显著减少，并且在手术后5-35天表现出持续的愈合痛觉过敏。将1%角叉菜胶注射到椎间孔中，可能引起DRG的炎症，也在手术后5-21天在受伤侧的后爪上产生对热的痛觉过敏。在体内进行了有髓背根纤维的细胞外电生理记录。自发活动存在于21.5%的纤维记录从DRG神经元损伤与慢性压缩相比，从未受伤的DRG神经元的1.98%。75.3%的自发活动纤维呈周期性和爆发性。这些神经元对机械刺激的敏感性大大增强，后放电时间延长。在响应TEA，局部应用于DRG，兴奋性反应引起的受伤，但不是未受伤的，DRG神经元。本实验模型的应用有助于我们进一步了解DRG慢性压迫引起下腰痛和坐骨神经痛的神经机制。(C)1998年国际疼痛研究协会。出版社：Elsevier Science B. V.
Under anesthesia and sterile surgery, a small stainless steel rod (4 mm in length and 0.5-0.8 mm in diameter) was inserted into the L5 intervertebral foramen in the rat, developing intervertebral foramen stenosis and hence producing a chronic steady compression of the dorsal root ganglion (DRG). The hind paw on the injured side exhibited a significant reduction in the latency of foot withdrawal to noxious heat and manifested a persistent heal hyperalgesia 5-35 days after surgery. Injection of 1% carrageenan into the intervertebral foramen, presumably causing inflammation of the DRG, also produced hyperalgesia to heat on the hind paw of the injured side 5-21 days after surgery. Extracellular electrophysiological recordings from myelinated dorsal root fibers were performed in vivo. Spontaneous activity was present in 21.5% of the fibers recorded from DRG neurons injured with chronic compression in contrast to 1.98% from uninjured DRG neurons. The pattern of spontaneous activity was periodic and bursting in 75.3% of the spontaneously active fibers. These neurons had a greatly enhanced sensitivity to mechanical stimulation of the injured DRG and a prolonged after discharge. In response to TEA, topically applied to the DRG, excitatory responses were evoked in the injured, but not the uninjured, DRG neurons. Application of this experimental model may further our understanding of the neural mechanisms by which chronic compression of DRG induces low back pain and sciatica. (C) 1998 International Association for the Study of Pain. Published by Elsevier Science B.V.