Aoki Yasuchika, Ohtori Seiji, Ino Hidetoshi, Douya Hideo, Ozawa Tomoyuki, Saito Tomoko, Moriya Hideshige, Takahashi Kazuhisa
Department of Orthopedic Surgery, Graduate School of Medicine, Chiba University, Chiba, Japan.
Spine (Phila Pa 1976). 2004 Dec 1;29(23):2621-6. doi: 10.1097/01.brs.0000146051.11574.b4.
The expression of growth-associated protein 43 (GAP-43), a marker of axonal growth, in the dorsal root ganglion (DRG) neurons innervating the lumbar intervertebral disc was assessed using the retrograde tracing method and immunohistochemistry.
To study whether disc inflammation affects GAP-43 expression in DRG neurons innervating the disc in rats.
Persistent inflammation and nerve ingrowth into the inner layer of degenerated discs can be a cause of discogenic pain. Although the presence of GAP-43-expressing nerve fibers in painful discs has been reported, the expression of GAP-43 in DRG neurons innervating the disc has not been studied.
Seven days after the application of Fluoro-Gold to the L5-L6 disc, 50 microL of saline (n = 10, control group) or complete Freund's adjuvant (n = 10, inflammatory group) was applied to the disc in rats. Ten days after the Fluoro-Gold application, T13-L5 DRGs were double-stained with GAP-43 and either calcitonin gene-related peptide or isolectin B4 (IB4).
The percentage of Fluoro-Gold-labeled neurons that were positive for GAP-43 was significantly higher in the inflammatory group (44%) than in the control group (24%, P < 0.001). In both groups, the majority of GAP-43-positive neurons were small and positive for calcitonin gene-related peptide but not IB4.
The present results suggest that disc inflammation potentially promotes axonal growth of DRG neurons innervating the disc. In light of the strong correlation between the expression of calcitonin gene-related peptide and nerve growth factor receptor, it is most likely that nerve growth factor-sensitive DRG neurons extend their axons following disc inflammation.
采用逆行示踪法和免疫组织化学方法，评估轴突生长标志物生长相关蛋白43（GAP - 43）在支配腰椎间盘的背根神经节（DRG）神经元中的表达。
研究椎间盘炎症是否影响大鼠支配椎间盘的DRG神经元中GAP - 43的表达。
持续炎症和神经向内生长进入退变椎间盘内层可能是椎间盘源性疼痛的一个原因。虽然已有报道在疼痛椎间盘中存在表达GAP - 43的神经纤维，但尚未研究支配椎间盘的DRG神经元中GAP - 43的表达情况。
将荧光金应用于L5 - L6椎间盘7天后，向大鼠椎间盘内注射50微升生理盐水（n = 10，对照组）或完全弗氏佐剂（n = 10，炎症组）。应用荧光金10天后，对T13 - L5背根神经节进行GAP - 43与降钙素基因相关肽或异凝集素B4（IB4）的双重染色。
炎症组中GAP - 43阳性的荧光金标记神经元百分比（44%）显著高于对照组（24%，P < 0.001）。在两组中，大多数GAP - 43阳性神经元较小，降钙素基因相关肽呈阳性，但IB4呈阴性。
目前的结果表明，椎间盘炎症可能促进支配椎间盘的DRG神经元的轴突生长。鉴于降钙素基因相关肽的表达与神经生长因子受体之间存在强相关性，很可能是对神经生长因子敏感的DRG神经元在椎间盘炎症后延伸其轴突。
