PMID- 27815510 OWN - NLM STAT- MEDLINE DCOM- 20170630 LR - 20180207 IS - 1470-8736 (Electronic) IS - 0143-5221 (Linking) VI - 130 IP - 24 DP - 2016 Dec 1 TI - Voltage-gated sodium channels and pain-related disorders. PG - 2257-2265 AB - Voltage-gated sodium channels (VGSCs) are heteromeric transmembrane protein complexes. Nine homologous members, SCN1A-11A, make up the VGSC gene family. Sodium channel isoforms display a wide range of kinetic properties endowing different neuronal types with distinctly varied firing properties. Among the VGSCs isoforms, Nav1.7, Nav1.8 and Nav1.9 are preferentially expressed in the peripheral nervous system. These isoforms are known to be crucial in the conduction of nociceptive stimuli with mutations in these channels thought to be the underlying cause of a variety of heritable pain disorders. This review provides an overview of the current literature concerning the role of VGSCs in the generation of pain and heritable pain disorders. CI - (c) 2016 The Author(s). published by Portland Press Limited on behalf of the Biochemical Society. FAU - Kanellopoulos, Alexandros H AU - Kanellopoulos AH AD - Molecular Nociception Group, Wolfson Institute for Biomedical Research, University College London, Gower Street, London WC1E 6BT, U.K. alexandros.kanellopoulos.13@ucl.ac.uk. FAU - Matsuyama, Ayako AU - Matsuyama A AD - Molecular Nociception Group, Wolfson Institute for Biomedical Research, University College London, Gower Street, London WC1E 6BT, U.K. LA - eng PT - Journal Article PT - Review PL - England TA - Clin Sci (Lond) JT - Clinical science (London, England : 1979) JID - 7905731 RN - 0 (Voltage-Gated Sodium Channels) SB - IM MH - Animals MH - Humans MH - Multigene Family MH - Neurons/metabolism MH - Pain/genetics/*metabolism MH - Voltage-Gated Sodium Channels/genetics/*metabolism OTO - NOTNLM OT - Nav1.7 OT - heritable disorders OT - pain OT - voltage-gated sodium channels EDAT- 2016/11/07 06:00 MHDA- 2017/07/01 06:00 CRDT- 2016/11/06 06:00 PHST- 2016/01/14 00:00 [received] PHST- 2016/09/15 00:00 [accepted] PHST- 2016/11/06 06:00 [entrez] PHST- 2016/11/07 06:00 [pubmed] PHST- 2017/07/01 06:00 [medline] AID - CS20160041 [pii] AID - 10.1042/CS20160041 [doi] PST - ppublish SO - Clin Sci (Lond). 2016 Dec 1;130(24):2257-2265. doi: 10.1042/CS20160041.