Univ. Paris-Sud, Laboratoire d'Anesthésie, UMR 788, Faculté de Médecine, F-94276 Le Kremlin Bicêtre, France.
Brain Behav Immun. 2010 May;24(4):652-9. doi: 10.1016/j.bbi.2010.01.013. Epub 2010 Feb 6.
Many pro-inflammatory cytokines are involved in the process of inflammatory pain. Bi directional axonal transport of Tumor Necrosis Factor-alpha (TNF-alpha) occurs in case of neuropathic pain induced by nerve ligation. We used an in vivo preparation with injection of carrageenan and fluorescent TNF-alpha in the territory of the saphenous nerve of rats to study this transport. We have shown that retrograde transport of TNF-alpha occurs after an inflammatory insult caused by the injection of carrageenan. This transport was likely mediated by the TNF receptor 1. A nerve block with bupivacaine totally abolishes the expression of the receptor in the dorsal root ganglion and the retrograde transport of TNF-alpha. In addition, bupivacaine at low concentrations (1-10 microM) was able to stop the axonal transport ex vivo. Tetrodotoxin was less efficacious for inhibiting the TNF-alpha transport and the rise in receptor expression and for inhibiting the axonal transport ex vivo. This may partly explain the efficacy of nerve blocks with bupivacaine to decrease the neurogenic inflammation and in a lower extent the long-term inhibition of hyperalgesic phenomenon observed in animals and in humans.
许多促炎细胞因子参与炎症性疼痛的过程。在神经结扎引起的神经性疼痛的情况下，肿瘤坏死因子-α（TNF-α）发生双向轴突运输。我们使用体内注射葡聚糖和荧光 TNF-α在大鼠隐神经区域的制备物来研究这种运输。我们已经表明，在注射葡聚糖引起的炎症损伤后，会发生 TNF-α的逆行运输。这种运输可能是由 TNF 受体 1 介导的。布比卡因神经阻滞完全消除了背根神经节中受体的表达和 TNF-α的逆行运输。此外，低浓度（1-10 μM）的布比卡因能够停止体外轴突运输。河豚毒素对抑制 TNF-α的运输和受体表达的增加以及体外轴突运输的抑制作用较小。这可以部分解释布比卡因神经阻滞降低神经源性炎症的有效性，以及在动物和人类中观察到的长期抑制痛觉过敏现象的程度较低。
