Department of Bioengineering, University of Pennsylvania, Philadelphia, PA 19104-6392, USA.
Spine (Phila Pa 1976). 2013 Mar 15;38(6):E325-31. doi: 10.1097/BRS.0b013e318285b5bb.
This study used retrograde neuronal tracing and immunohistochemistry to identify neurons innervating the C6-C7 facet joint and those expressing calcitonin gene-related peptide (CGRP) in the dorsal root ganglion (DRG) of rats after painful cervical facet joint injury.
The objective of this study was to characterize the innervation of the C6-C7 facet joint after painful joint injury in the rat.
The cervical facet joint is a source of neck pain, and its loading can initiate persistent pain. CGRP is a nociceptive neurotransmitter; peptidergic afferents have been identified in the facet joint's capsule. Although studies suggest that facet joint injury alters CGRP expression in joint afferents, the distribution of neurons innervating the C6-C7 facet joint and their expression of CGRP after a painful joint injury have not been investigated.
Holtzman rats (Harlan Sprague-Dawley, Indianapolis, IN) received an intra-articular injection of cholera toxin subunit B in the C6-C7 facet joints. After injection, subgroups underwent either a painful joint distraction or sham procedure. Mechanical sensitivity was assessed, and immunohistochemical techniques were used to quantify CGRP expression and cholera toxin subunit B labeling in the C5-C8 DRGs.
Facet joint distraction-induced (P ≤ 0.0002) hypersensitivity. Neurons labeled by the joint injection were identified in the C5-C8 DRGs. Significantly, more (P ≤ 0.0001) cholera toxin subunit B-positive neurons were identified in the C7 DRG than any other level. At C7, 54.4% ± 15.3% of those neurons were also CGRP-positive, whereas only 41.5% ± 5.4% of all neurons were CGRP-positive; this difference was significant (P = 0.0084).
The greatest number of afferents from the C6-C7 facet joint has cell bodies in the C7 DRG, implicating this level as the most relevant for pain from this joint. In addition, peptidergic afferents seem to have an important role in facet joint-mediated pain.
本研究采用逆行神经元追踪和免疫组织化学方法,鉴定在大鼠疼痛性颈椎小关节损伤后,支配 C6-C7 小关节的神经元和背根神经节(DRG)中表达降钙素基因相关肽(CGRP)的神经元。
本研究旨在描述大鼠疼痛性小关节损伤后 C6-C7 小关节的神经支配。
颈椎小关节是颈部疼痛的一个来源,其负荷可引发持续性疼痛。CGRP 是一种伤害感受性神经递质;已经在小关节囊的肽能传入纤维中鉴定出 CGRP。尽管研究表明小关节损伤改变了关节传入纤维中 CGRP 的表达,但支配 C6-C7 小关节的神经元的分布及其在疼痛性关节损伤后的 CGRP 表达尚未得到研究。
哈茨曼大鼠(印第安纳州印第安纳波利斯市哈伦斯·斯普雷格·道利公司)在 C6-C7 小关节内注射霍乱毒素亚单位 B。注射后,亚组接受疼痛性关节分离或假手术。评估机械敏感性,并使用免疫组织化学技术定量 C5-C8 DRG 中的 CGRP 表达和霍乱毒素亚单位 B 标记。
小关节分离诱导的(P ≤ 0.0002)过敏。在 C5-C8 DRG 中鉴定出由关节注射标记的神经元。重要的是,C7 DRG 中鉴定出的霍乱毒素亚单位 B 阳性神经元明显多于任何其他水平(P ≤ 0.0001)。在 C7 处,54.4%±15.3%的神经元也是 CGRP 阳性,而只有 41.5%±5.4%的神经元是 CGRP 阳性;这种差异具有统计学意义(P = 0.0084)。
来自 C6-C7 小关节的最大数量的传入纤维在 C7 DRG 中有细胞体,这表明该水平与该关节的疼痛最相关。此外,肽能传入纤维似乎在小关节介导的疼痛中起重要作用。