Peripheral inflammation induces up-regulation of TRPV2 expression in rat DRG

Peripheral inflammation induces up-regulation of TRPV2 expression in rat DRG
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DOI:
10.1016/j.pain.2005.10.002
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发表时间:
2005-12-15
期刊:
影响因子:
7.4
通讯作者:
Tanaka, M
Tanaka, M
中科院分区:
医学1区
文献类型:
--
作者:
Shimosato, G;Amaya, F;Tanaka, M

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瞬时受体电位香草酸亚家族成员2(TRPV2)是由高于52摄氏度的温度激活的阳离子通道。为了分析TRPV2对炎症诱导的痛觉过敏的发展的贡献,在足底注射完全弗氏佐剂(CFA)后分析TRPV2在初级感觉神经元中的表达。使用特异性抗体,在炎症后鉴定了TRPV2表达神经元的增加。TRPV2的表达集中在一个子集的中型背根神经节神经元,独立的瞬时受体电位香草素亚家族成员1(TRPV1)的表达。在炎症后观察到TRPV2的类似分布。足底注射神经生长因子可增加TRPV1的表达,但不增加TRPV2的表达,这表明TRPV2表达的诱导是由与TRPV1不同的机制驱动的。通过树脂毒素对TRPV1进行化学脱敏后的热痛觉过敏评估表明TRPV2在高温(> 56 ℃)下的炎症中可能起作用。这些结果表明,TRPV2上调有助于炎症期间的外周敏化,并负责对有害高温刺激的疼痛超敏反应。(c)2005年国际疼痛研究协会。Elsevier B.V.出版,保留所有权利。
The transient receptor potential vanilloid subfamily member 2 (TRPV2) is a cation channel activated by temperatures above 52 degrees C. To analyze the contribution of TRPV2 to the development of inflammation-induced hyperalgesia, the expression of TRPV2 in primary sensory neurons was analyzed after intraplantar injection of complete Freund's adjuvant (CFA). Using specific antibodies, an increase in TRPV2-expressing neurons was identified after inflammation. TRPV2 expression is concentrated in a subset of medium-sized dorsal root ganglion neurons, independent of transient receptor potential vanilloid subfamily member 1 (TRPV1) expression. A similar distribution of TRPV2 was observed after inflammation. Intraplantar injection of nerve growth factor increased TRPV1 expression but not TRPV2, suggesting that induction of TRPV2 expression is driven by a mechanism distinct from that for TRPV1. Heat hyperalgesia assessment after chemical desensitization of TRPV1 by resiniferatoxin demonstrates a possible role for TRPV2 in inflammation at high temperatures (> 56 degrees C). These results suggest that TRPV2 upregulation contributes to peripheral sensitization during inflammation and is responsible for pain hypersensitivity to noxious high temperature stimuli. (c) 2005 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.