4.4 Article

The Roles of Sodium Channels in Nociception: Implications for Mechanisms of Neuropathic Pain

期刊

PAIN MEDICINE
卷 12, 期 -, 页码 S93-S99

出版社

WILEY-BLACKWELL
DOI: 10.1111/j.1526-4637.2011.01158.x

关键词

Animal Models; Nav1.7; Nav1.8; Nav1.9; Neuropathic Pain; Null Mutants; Voltage-Gated Sodium Channels

资金

  1. Endo Pharmaceuticals Inc.
  2. Wellcome Trust
  3. BBSRC [BB/F000227/1] Funding Source: UKRI
  4. MRC [G0901905] Funding Source: UKRI
  5. Biotechnology and Biological Sciences Research Council [BB/F000227/1] Funding Source: researchfish
  6. Medical Research Council [G0901905] Funding Source: researchfish

向作者/读者索取更多资源

Animal models have provided useful insights into the development and treatment of neuropathic pain. New genetic data from both human studies and transgenic mouse models suggest that specific voltage-gated sodium channel subtypes are associated with specific types of pain and, as such, may be useful analgesic drug targets for a variety of pain types including neuropathic pain. Global voltage-gated sodium channel blockers such as lidocaine have proven efficacy in treating pain but can be limited by adverse effects when administered systemically. Selective sodium channel blockers targeting channels at the periphery (Nav1.7, Nav1.8, and Nav1.9) could potentially reduce the side effect profile. Individual isoforms of voltage-gated sodium channels have been linked to particular types of pain. Nav1.7 is a useful target for ameliorating acute mechanical pain and inflammatory pain, and strong evidence also suggests that Nav1.9 could be targeted for treating inflammatory pain. Selective blockers of Nav1.8 could also have clinical benefit for visceral pain. Although there is no association between a single sodium channel isoform and neuropathic pain, combined blockade of peripherally expressed isoforms Nav1.7, Nav1.8, and Nav1.9 may prove useful.

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