Sodium Channels in Normal and Pathological Pain

Author:

Dib-Hajj Sulayman D.123,Cummins Theodore R.4,Black Joel A.123,Waxman Stephen G.123

Affiliation:

1. Department of Neurology and, Veterans Affairs Connecticut Healthcare System, West Haven, Connecticut 06516

2. Center for Neuroscience and Regeneration Research, Yale University School of Medicine, New Haven, Connecticut 06510

3. Rehabilitation Research Center, Veterans Affairs Connecticut Healthcare System, West Haven, Connecticut 06516

4. Department of Pharmacology and Toxicology, Stark Neurosciences Institute, Indiana University School of Medicine, Indianapolis, Indiana 46202;

Abstract

Nociception is essential for survival whereas pathological pain is maladaptive and often unresponsive to pharmacotherapy. Voltage-gated sodium channels, Nav1.1–Nav1.9, are essential for generation and conduction of electrical impulses in excitable cells. Human and animal studies have identified several channels as pivotal for signal transmission along the pain axis, including Nav1.3, Nav1.7, Nav1.8, and Nav1.9, with the latter three preferentially expressed in peripheral sensory neurons and Nav1.3 being upregulated along pain-signaling pathways after nervous system injuries. Nav1.7 is of special interest because it has been linked to a spectrum of inherited human pain disorders. Here we review the contribution of these sodium channel isoforms to pain.

Publisher

Annual Reviews

Subject

General Neuroscience

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