Spinal nerve ligation induces transient upregulation of tumor necrosis factor receptors 1 and 2 in injured and adjacent uninjured dorsal root ganglia in the rat
Spinal nerve ligation induces transient upregulation of tumor necrosis factor receptors 1 and 2 in injured and adjacent uninjured dorsal root ganglia in the rat
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DOI：
10.1016/s0304-3940(03)00695-5
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发表时间：
2003-08-28
影响因子：
2.5
通讯作者：
Shubayev, VI
中科院分区：
文献类型：
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作者：
Schäfers, M;Sorkin, LS;Shubayev, VI
有证据表明肿瘤坏死因子-α（TNF）在神经性疼痛中的作用。我们相关的疼痛行为，响应机械刺激与免疫反应的TNF受体（TNFR）I和2在6，24，76和120小时后L5和L 6脊神经结扎（SNL）。SNL后6 h内，L4和L5皮区均开始出现异常性疼痛，24 h达到峰值。在L5（受损）背根神经节（DRG），TNFR I和TNFR 2水平显示双峰增加，在SNL后6和120小时达到峰值。在L4（未损伤）DRG中，TNFR I和TNFR 2免疫反应性在24 h达到峰值，到120 h恢复到基础水平。TNFR在受损和邻近未受损DRG神经元中的上调可能是介导增强的TNF效应所必需的，从而有助于疼痛相关行为的发展。(C)2003爱思唯尔爱尔兰有限公司保留所有权利。
Evidence indicates a role for tumor necrosis factor-alpha (TNF) in neuropathic pain. We correlated pain behavior in response to mechanical stimulation with immunoreactivity for TNF receptor (TNFR) I and 2 at 6, 24, 76 and 120 h following L5 and L6 spinal nerve ligation (SNL). Allodynia began in both L4 and L5 dermatomes within 6 h following SNL, peaking by 24 h. In L5 (injured) dorsal root Ganglia (DRG), TNFR I and TNFR2 levels displayed a bimodal increase, peaking at 6 and 120 h after SNL. In L4 (uninjured) DRG, TNFR I and TNFR2 immunoreactivity peaked at 24 h returning to basal levels by 120 h. TNFR upregulation in injured and adjacent uninjured DRG neurons may be essential for mediating enhanced TNF effects and thus contribute to the development of pain-related behavior. (C) 2003 Elsevier Ireland Ltd. All rights reserved.