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揭开神经生长因子介导的伤害性感觉神经元敏化的故事:是通过酪氨酸激酶受体(Trks)激活还是失活?

Unraveling the story of NGF-mediated sensitization of nociceptive sensory neurons: ON or OFF the Trks?

作者信息

Nicol Grant D, Vasko Michael R

机构信息

Department of Pharmacology and Toxicology, Indiana University School of Medicine, Indianapolis, Indiana 46202, USA.

出版信息

Mol Interv. 2007 Feb;7(1):26-41. doi: 10.1124/mi.7.1.6.

DOI:10.1124/mi.7.1.6
PMID:17339604
Abstract

Nerve Growth Factor (NGF) is produced by and affects a number of immune and inflammatory cells. As part of the inflammatory response, NGF directly or indirectly alters the sensitivity of small diameter sensory neurons that communicate noxious information. The question remains as to the receptors and intracellular signaling cascades that mediate this sensitizing action of NGF. Although the general consensus is that NGF produces peripheral sensitization by activating TrkA, recent work suggests that p75 also contributes. Thus, both NGF receptors appear to contribute to peripheral sensitization although whether they act independently or together remains to be determined. Furthermore, controversy exists as to the downstream signaling pathways involved in NGF-induced peripheral sensitization.

摘要

神经生长因子(NGF)由多种免疫和炎症细胞产生并对其产生影响。作为炎症反应的一部分,NGF直接或间接改变传递有害信息的小直径感觉神经元的敏感性。关于介导NGF这种致敏作用的受体和细胞内信号级联反应的问题依然存在。尽管普遍的共识是NGF通过激活TrkA产生外周致敏,但最近的研究表明p75也有作用。因此,两种NGF受体似乎都对外周致敏有作用,不过它们是独立发挥作用还是共同发挥作用仍有待确定。此外,关于NGF诱导外周致敏所涉及的下游信号通路也存在争议。

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