Receptor-targeting mechanisms of pain-causing toxins: How ow?

被引：48

作者：

Bohlen, Christopher J. ^{[1
]}

Julius, David ^{[1
]}

机构：

[1] Univ Calif San Francisco, Dept Physiol, San Francisco, CA 94158 USA

来源：

TOXICON | 2012年 / 60卷 / 03期

关键词：

Pain; Venom; TRPV1; ASIC; Multivalent toxin; Multimeric toxin; SENSING ION CHANNELS; GATED NA+ CHANNELS; CAPSAICIN RECEPTOR; VANILLOID RECEPTOR-1; POTASSIUM CHANNELS; TARANTULA TOXINS; VOLTAGE SENSORS; SPIDER VENOM; IMPAIRED NOCICEPTION; INFLAMMATORY PAIN;

D O I：

10.1016/j.toxicon.2012.04.336

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

Venoms often target vital processes to cause paralysis or death, but many types of venom also elicit notoriously intense pain. While these pain-producing effects can result as a byproduct of generalized tissue trauma, there are now multiple examples of venom-derived toxins that target somatosensory nerve terminals in order to activate nociceptive (pain-sensing) neural pathways. Intriguingly, investigation of the venom components that are responsible for evoking pain has revealed novel roles and/or configurations of well-studied toxin motifs. This review serves to highlight pain-producing toxins that target the capsaicin receptor, TRPV1, or members of the acid-sensing ion channel family, and to discuss the utility of venom-derived multivalent and multimeric complexes. (C) 2012 Elsevier Ltd. All rights reserved.

引用

页码：254 / 264

页数：11

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