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降钙素基因相关肽免疫反应性背根神经节神经元支配腰椎小关节显示大鼠的表型炎症转换。

Phenotypic inflammation switch in rats shown by calcitonin gene-related peptide immunoreactive dorsal root ganglion neurons innervating the lumbar facet joints.

作者信息

Ohtori S, Takahashi K, Chiba T, Yamagata M, Sameda H, Moriya H

机构信息

Third Department of Anatomy, School of Medicine, Chiba University, Chiba, Japan.

出版信息

Spine (Phila Pa 1976). 2001 May 1;26(9):1009-13. doi: 10.1097/00007632-200105010-00005.

Abstract

STUDY DESIGN

The changes in dorsal root ganglion neurons innervating the L5-L6 facet joint were studied using the retrograde neurotransport method and the immunohistochemistry of calcitonin gene-related peptide in an inflammatory model of rats.

OBJECTIVES

To determine by inflammatory stimulation the changes in calcitonin gene-related peptide-immunoreactive dorsal root ganglion neurons innervating the L5-L6 facet.

SUMMARY OF BACKGROUND DATA

The rat L5-L6 facet joint is innervated from L1-L5 dorsal root ganglia. The presence of calcitonin gene-related peptide-immunoreactive dorsal root ganglion neurons innervating the L5-L6 facet joint has been confirmed, but the changes in the number and distribution of these neurons caused by inflammation have not been studied.

METHODS

Retrograde transport of fluorogold was used in 20 rats: 10 in the control group and 10 in the inflammatory group. Using the dorsal approach, fluorogold crystals were injected into the left L5-L6 facet joint. Then 5 days after application, complete Freund's adjuvant (50 microg Mycobacterium butyricum in oil saline emulsion) was injected into the same L5-L6 facet joint (inflammatory group). Of the total fluorogold-labeled dorsal root ganglion neurons from T13-L6, the number and cross-sectional area of the cell profiles of fluorogold-labeled, calcitonin gene-related peptide-immunoreactive neurons in the bilateral dorsal root ganglia of both groups were evaluated.

RESULTS

Fluorogold-labeled neurons were distributed throughout the ipsilateral dorsal root ganglia from L1-L5 in both groups. Of the fluorogold-labeled neurons, the ratios of the calcitonin gene-related peptide-immunoreactive L1, L2, L3, L4, and L5 dorsal root ganglion neurons, respectively, were 17%, 24%, 44%, 56%, and 50% in the control group and 50%, 39%, 51%, 61%, and 56% in the inflammatory group. The ratios of the calcitonin gene-related peptide-immunoreactive L1 and L2 dorsal root ganglion neurons labeled by fluorogold were significantly higher in the inflammatory group than in the control group (P < 0.05). The mean cross-sectional area of fluorogold-labeled, calcitonin gene-related peptide-immunoreactive cells from L1-L5 dorsal root ganglia increased from 621 +/- 64 microm2 to 893 +/- 63 microm2 in the inflammatory group (P < 0.01).

CONCLUSIONS

The ratio of fluorogold-labeled, calcitonin gene-related peptide-immunoreactive neurons was significantly higher in the L1 and L2 dorsal root ganglia of the inflammatory group than in those of the control group, and the average cross-sectional area of the cells from L1-L5 dorsal root ganglion increased. Associated with the inflammation in the facet joints, the change in calcitonin gene-related peptide-immunoreactive neuron distribution and the phenotypic switch to large neurons may complicate the mechanism of facet joint inflammatory pain.

摘要

研究设计

采用逆行神经运输法和降钙素基因相关肽免疫组织化学方法,在大鼠炎症模型中研究支配L5-L6小关节的背根神经节神经元的变化。

目的

通过炎症刺激确定支配L5-L6小关节的降钙素基因相关肽免疫反应性背根神经节神经元的变化。

背景数据总结

大鼠L5-L6小关节由L1-L5背根神经节支配。已证实存在支配L5-L6小关节的降钙素基因相关肽免疫反应性背根神经节神经元,但尚未研究炎症导致的这些神经元数量和分布的变化。

方法

对20只大鼠采用荧光金逆行运输法:对照组10只,炎症组10只。采用背侧入路,将荧光金晶体注射到左侧L5-L6小关节。然后在应用5天后,将完全弗氏佐剂(50微克丁酸分枝杆菌油盐水乳剂)注射到同一L5-L6小关节(炎症组)。在T13-L6的所有荧光金标记的背根神经节神经元中,评估两组双侧背根神经节中荧光金标记的、降钙素基因相关肽免疫反应性神经元细胞轮廓的数量和横截面积。

结果

两组中荧光金标记的神经元均分布在同侧L1-L5背根神经节。在荧光金标记的神经元中,对照组中降钙素基因相关肽免疫反应性L1、L2、L3、L4和L5背根神经节神经元的比例分别为17%、24%、44%、56%和50%,炎症组分别为50%、39%、51%、61%和56%。炎症组中荧光金标记的降钙素基因相关肽免疫反应性L1和L2背根神经节神经元的比例显著高于对照组(P<0.05)。炎症组中L1-L5背根神经节中荧光金标记的、降钙素基因相关肽免疫反应性细胞的平均横截面积从621±64平方微米增加到893±63平方微米(P<0.01)。

结论

炎症组L1和L2背根神经节中荧光金标记的、降钙素基因相关肽免疫反应性神经元的比例显著高于对照组,且L1-L5背根神经节细胞的平均横截面积增加。与小关节炎症相关,降钙素基因相关肽免疫反应性神经元分布的变化以及向大神经元的表型转换可能使小关节炎症性疼痛的机制复杂化。

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