Peripheral capsaicin receptors increase in the inflamed rat hindpaw: a possible mechanism for peripheral sensitization
Peripheral capsaicin receptors increase in the inflamed rat hindpaw: a possible mechanism for peripheral sensitization
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DOI：
10.1016/s0304-3940(01)02093-6
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发表时间：
2001-09-07
影响因子：
2.5
通讯作者：
Coggeshall, RE
中科院分区：
文献类型：
--
作者：
Carlton, SM;Coggeshall, RE
辣椒素受体1（VR 1）被辣椒素、热和质子激活，位于初级感觉神经元上。本研究调查是否VR 1增加发炎后爪，从而有助于外周敏化和热痛觉过敏的特征发炎状态。在将完全弗氏佐剂足底注射到一只后爪中后48小时，与正常后爪（17.1 +/-2.6%）相比，发炎后爪（32.8 +/-5.9%）的指神经中VR 1标记的无髓鞘轴突的比例显著增加（t检验，P < 0.01）。在正常和炎症大鼠中标记了少数小直径的有髓鞘轴突，炎症后百分比没有变化。这些数据表明，表达VR 1的无髓鞘感觉轴突数量的增加可能是炎症中伤害感受器外周致敏的一种机制。(C)2001爱思唯尔科学爱尔兰有限公司保留所有权利。
The vanilloid receptor-1 (VR1) is activated by capsaicin, heat and protons and is localized on primary sensory neurons. The present study investigates whether VR1 increases in the inflamed hindpaw thereby contributing to the peripheral sensitization and heat hyperalgesia that characterizes the inflamed state. Forty-eight hours after intraplantar injection of Complete Freund's Adjuvant into one hindpaw, there is a significant increase in the proportion of VR1-labeled unmyelinated axons in digital nerves in the inflamed (32.8 +/- 5.9%) compared to normal (17.1 +/- 2.6%) hindpaws (t-test, P < 0.01). A few, small diameter myelinated axons are labeled in normal and inflamed rats with no change in percentages following inflammation. The data suggest that an increase in number of unmyelinated sensory axons expressing VR1 may be one mechanism underlying peripheral sensitization of nociceptors in inflammation. (C) 2001 Elsevier Science Ireland Ltd. All rights reserved.