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The role of sodium channels in neuropathic pain

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Rogers, Marc, Tang, Lam, Madge, David J. and Stevens, Edward B. (2006) The role of sodium channels in neuropathic pain. SEMINARS IN CELL & DEVELOPMENTAL BIOLOGY, 17 (5). pp. 571-581. ISSN 1084-9521

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Official URL: http://dx.doi.org/10.1016/j.semedb.2006.10.009

Abstract

Our knowledge of the ion channels, receptors and signalling mechanisms involved in pain pathophysiology, and which specific channels play a role in subtypes of pain such as neuropathic and inflammatory pain, has expanded considerably in recent years. It is now clear that in the neuropathic state the expression of certain channels is modified, and that these changes underlie the plasticity of responses that occur to generate inappropriate pain signals from normally trivial inputs. Pain is modulated by a subset of the voltage-gated sodium channels, including Nav1.3, Nav1.7, Nav1.8 and Nav1.9. These isoforms display unique expression patterns within specific tissues, and are either up- or down-regulated upon injury to the nervous system. Here we describe our current understanding of the roles of sodium channels in pain and nociceptive information processing, with a particular emphasis on neuropathic pain and drugs useful for the treatment of neuropathic pain that act through mechanisms involving block of sodium channels. One of the future challenges in the development of novel sodium channel blockers is to design and synthesise isoform-selective channel inhibitors. This should provide substantial benefits over existing pain treatments. (c) 2006 Elsevier Ltd. All rights reserved.

Item Type: Journal Item
Subjects: Q Science > QH Natural history > QH301 Biology
Journal or Publication Title: SEMINARS IN CELL & DEVELOPMENTAL BIOLOGY
Publisher: ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD
ISSN: 1084-9521
Date: October 2006
Volume: 17
Number: 5
Number of Pages: 11
Page Range: pp. 571-581
Identification Number: 10.1016/j.semedb.2006.10.009
Publication Status: Published
URI: http://wrap.warwick.ac.uk/id/eprint/32377

Data sourced from Thomson Reuters' Web of Knowledge

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