Tseng To-Jung, Hsieh Yu-Lin, Hsieh Sung-Tsang
Department of Anatomy and Cell Biology, National Taiwan University College of Medicine, and Department of Neurology, National Taiwan University Hospital, Taipei 10051, Taiwan.
Exp Neurol. 2007 Jul;206(1):17-23. doi: 10.1016/j.expneurol.2007.04.006. Epub 2007 May 4.
Injury-induced neuropathic pain is related to changes in the central terminals of dorsal root ganglia neurons, i.e., dorsal horn plasticity. We investigated the influences of decompression by removing ligatures producing chronic constriction injury (CCI) in Sprague-Dawley rats at postoperative week (POW) 4, the decompression group; for comparison, all ligatures remained through the experimental period in the CCI group. The effect was evaluated with extracellular signal-regulated kinase (ERK) activation in the dorsal horn, i.e., number of phosphorylated ERK (+) cells in the dorsal horn. At POW 1, the dorsal horn indexes had increased to a similar degree in both groups (2.40+/-0.58 vs. 2.27+/-0.36, p=0.73). At POW 8, thermal hyperalgesia and mechanical allodynia had completely disappeared with a normalization of dorsal horn index (1.17+/-0.11 vs. 1.02+/-0.12 at POW 0, p=0.07) in the decompression group; in contrast, the dorsal horn index remained elevated in the CCI group (2.48+/-0.30, p<0.001) with persistent neuropathic pain behaviors at POW 8. This report suggests that ERK activation in the dorsal horn is correlated with neuropathic pain behaviors and its normalization reflects the reversal of neuropathic pain behaviors after decompression.
损伤诱导的神经性疼痛与背根神经节神经元中枢终末的变化有关，即脊髓背角可塑性。我们研究了在术后第4周（POW 4）通过移除产生慢性压迫性损伤（CCI）的结扎线进行减压的影响，减压组；作为对照，CCI组在整个实验期间保留所有结扎线。通过脊髓背角中的细胞外信号调节激酶（ERK）激活来评估效果，即脊髓背角中磷酸化ERK（+）细胞的数量。在POW 1时，两组的脊髓背角指数均升高至相似程度（2.40±0.58对2.27±0.36，p = 0.73）。在POW 8时，减压组的热痛觉过敏和机械性异常性疼痛完全消失，脊髓背角指数恢复正常（POW 0时为1.17±0.11对1.02±0.12，p = 0.07）；相比之下，CCI组的脊髓背角指数仍升高（2.48±0.30，p<0.001），在POW 8时仍存在神经性疼痛行为。本报告表明，脊髓背角中的ERK激活与神经性疼痛行为相关，其恢复正常反映了减压后神经性疼痛行为的逆转。
