Enhanced excitability of nociceptive trigeminal ganglion neurons by satellite glial cytokine following peripheral inflammation
Enhanced excitability of nociceptive trigeminal ganglion neurons by satellite glial cytokine following peripheral inflammation
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DOI：
10.1016/j.pain.2006.10.007
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发表时间：
2007-05-01
期刊：
影响因子：
7.4
通讯作者：
Matsumoto, Shigeji
中科院分区：
文献类型：
--
作者：
Takeda, Mamoru;Tanimoto, Takeshi;Matsumoto, Shigeji
周围神经损伤激活卫星细胞产生介导炎症和痛觉过敏的白细胞介素1 β（IL-1 β）。本研究探讨了卫星胶质细胞的激活通过IL-1 β调节炎症后三叉神经节（TRG）神经元兴奋性的假设。通过将完全弗氏佐剂（CFA）注射到须垫区域中来诱导炎症。对机械刺激的逃避阈值，炎症大鼠明显低于对照组。CFA注射后两天，与对照组相比，被胶质细胞酸性蛋白（GFAP）-/IL-1 β免疫反应细胞包围的TRG神经元的平均百分比显著增加。GFAP和IL-1 β免疫反应性在同一细胞中共表达。荧光金（FG）标记确定炎症部位。FG标记的IL-1受体I型（IL-1RI）TRG神经元的数量在炎症大鼠显着大于对照组。在FG标记的小TRG神经元中，炎症大鼠中IL-1 β（1 nM）诱导的去极化的大小大于对照组。与对照组相比，IL-1 β应用显著增加了炎症大鼠神经元中去极化脉冲诱发的放电率。通过用IL-1RI拮抗剂处理消除了对IL-1 β的反应。这些结果表明，炎症后卫星胶质细胞的激活通过IL-1 β调节小直径TRG神经元的兴奋性，并且索马体内IL-1 RI的上调可能有助于炎症性痛敏的潜在机制。因此，IL-1 β阻滞剂是预防三叉神经痛敏的潜在治疗药物。(c)2006年国际疼痛研究协会。Elsevier B.V.出版，保留所有权利。
Peripheral nerve injury activates satellite cells to produce interleukin 1 beta (IL-1 beta) which mediates inflammation and hyperalgesia. This study investigated the hypothesis that activation of satellite glial cells modulates the excitability of trigeminal ganglion (TRG) neurons via IL-1 beta following inflammation. Inflammation was induced by injection of complete Freund's adjuvant (CFA) into the whisker pad area. The threshold for escape from mechanical stimulation applied to the whisker pad in inflamed rats was significantly lower than that in control. Two days post-CFA injection, the mean percentage of TRG neurons encircled by glial fibrillary acidic protein (GFAP)-/IL-1 beta-immunoreactive cells was significantly increased compared to controls. GFAP and IL-1 beta immunoreactivities were coexpressed in the same cells. Fluorogold (FG) labeling identified the site of inflammation. The number of FG-labeled IL-receptor type I (IL-1RI) TRG neurons in inflamed rats was significantly greater than in controls. In FG-labeled small TRG neurons, the size of IL-1 beta (1 nM) induced-depolarization in inflamed rats was larger than in controls. IL-1 beta application significantly increased firing rates evoked by depolarizing pulses in the neurons of inflamed rats, compared to controls. The response to IL-1 beta was abolished by treatment with the IL-1RI antagonist. These results suggest that activation of satellite glial cells modulates the excitability of small-diameter TRG neurons via IL-1 beta following inflammation, and that the upregulation of IL-1RI in the soma may contribute to the mechanism underlying inflammatory hyperalgesia. Therefore IL-1 beta blockers are potential therapeutic agents for prevention of trigeminal hyperalgesia. (c) 2006 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.