Ma W, Bisby M A
Department of Physiology, Botterell Hall, Faculty of Medicine, Queen's University, Kingston, Ontario, Canada.
Brain Res. 1998 Jun 29;797(2):243-54. doi: 10.1016/s0006-8993(98)00380-1.
Nuclear factor kappa B (NFkappaB) is a transcription factor which can be activated by some neurotrophic factors and cytokines, and then translocated into the nucleus. We examined NFkappaB immunoreactivity (IR) in L4 and L5 dorsal root ganglion (DRG) cells of normal rats, and 2 weeks after complete sciatic nerve transection (CSNT), partial sciatic nerve ligation (PSNL) and chronic constriction injury (CCI). In the normal DRG, 45% of the neurons were NFkappaB-IR (IR in cytoplasm only or in both cytoplasm and nucleus). Only 18% were activated NFkappaB-IR cells (IR in both cytoplasm and nucleus). Two weeks after CSNT, PSNL and CCI, there was no significant difference in the percentages of NFkappaB-IR neurons between the ipsilateral and contralateral DRG. However, the percentages of the activated NFkappaB-IR neurons in the ipsilateral DRG of PSNL (30%) and CCI (33%) rats, but not in CSNT (24%) rats, were significantly increased, compared with the contralateral DRG. Ultrastructurally, NFkappaB-IR was localized to the endoplasmic reticulum and Golgi apparatus. In activated cells, IR was also observed in the nuclei. Two weeks after CCI, NFkappaB-IR was stronger in the axons and Schwann cells in the proximal stump of the injured sciatic nerves than in uninjured contralateral nerves. In some Schwann cells surrounding unmyelinated fibers, the nuclei were also NFkappaB-IR, suggesting that these cells were activated by CCI. NFkappaB activation increased in DRG neurons and Schwann cells 2 weeks following partial sciatic injuries, possibly in response to cytokines and neurotrophins produced by endoneurial cells in the partially injured nerve during Wallerian degeneration.
核因子κB（NFκB）是一种转录因子，可被某些神经营养因子和细胞因子激活，然后转位至细胞核。我们检测了正常大鼠以及坐骨神经完全横断（CSNT）、部分坐骨神经结扎（PSNL）和慢性压迫性损伤（CCI）2周后L4和L5背根神经节（DRG）细胞中的NFκB免疫反应性（IR）。在正常DRG中，45%的神经元为NFκB-IR（仅细胞质或细胞质和细胞核中均有IR）。仅18%为活化的NFκB-IR细胞（细胞质和细胞核中均有IR）。CSNT、PSNL和CCI后2周，同侧和对侧DRG中NFκB-IR神经元的百分比无显著差异。然而，与对侧DRG相比，PSNL（30%）和CCI（33%）大鼠同侧DRG中活化的NFκB-IR神经元百分比显著增加，而CSNT（24%）大鼠则未增加。超微结构上，NFκB-IR定位于内质网和高尔基体。在活化细胞中，细胞核中也观察到IR。CCI后2周，损伤坐骨神经近端残端的轴突和雪旺细胞中的NFκB-IR比未损伤的对侧神经更强。在一些围绕无髓纤维的雪旺细胞中，细胞核也为NFκB-IR，表明这些细胞被CCI激活。部分坐骨神经损伤后2周，DRG神经元和雪旺细胞中的NFκB活化增加，可能是对沃勒变性期间部分损伤神经中神经内膜细胞产生的细胞因子和神经营养因子的反应。
