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外周炎症诱导大鼠背根神经节中TRPV2表达上调。

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

作者信息

Shimosato Goshun, Amaya Fumimasa, Ueda Masashi, Tanaka Yoshifumi, Decosterd Isabelle, Tanaka Masaki

机构信息

Department of Anesthesiology, Kyoto Prefectural University of Medicine, 465 Kajiicho, Kamigyo-ku, Kyoto 602-8566, Japan Department of Anesthesiology Pain Research Group, Anesthesiology Department, Lausanne University Hospital (CHUV), Lausanne, Switzerland Department of Cell Biology and Morphology (DBCM), Faculty of Biology and Medicine, Lausanne University, Lausanne, Switzerland Department of Anatomy, Kyoto Prefectural University of Medicine, Kyoto, Japan.

出版信息

Pain. 2005 Dec 15;119(1-3):225-232. doi: 10.1016/j.pain.2005.10.002. Epub 2005 Nov 17.

DOI:10.1016/j.pain.2005.10.002
PMID:16298071
Abstract

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.

摘要

瞬时受体电位香草酸亚家族成员2(TRPV2)是一种由高于52摄氏度的温度激活的阳离子通道。为了分析TRPV2在炎症诱导的痛觉过敏发展中的作用,在足底注射完全弗氏佐剂(CFA)后,分析了初级感觉神经元中TRPV2的表达。使用特异性抗体,炎症后发现表达TRPV2的神经元增加。TRPV2表达集中在中等大小的背根神经节神经元亚群中,与瞬时受体电位香草酸亚家族成员1(TRPV1)的表达无关。炎症后观察到TRPV2有类似的分布。足底注射神经生长因子增加了TRPV1的表达,但未增加TRPV2的表达,这表明TRPV2表达的诱导是由一种不同于TRPV1的机制驱动的。在用树脂毒素对TRPV1进行化学脱敏后进行热痛觉过敏评估,结果表明TRPV2在高温(>56摄氏度)炎症中可能发挥作用。这些结果表明,TRPV2上调有助于炎症期间的外周敏化,并导致对有害高温刺激的疼痛超敏反应。

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