The role of sodium channels in chronic pain

Authors

  • Simon R. Levinson PhD,

    Corresponding author
    1. Department of Physiology and Biophysics, University of Colorado School of Medicine, Aurora, Colorado 80045, USA
    • Department of Physiology and Biophysics, University of Colorado School of Medicine, Aurora, Colorado 80045, USA
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  • Songjiang Luo PhD, DDS,

    1. Department of Comprehensive Dentistry, University of Texas Health Science Center at San Antonio, San Antonio, Texas, USA
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  • Michael A. Henry PhD, DDS

    1. Department of Endodontics, University of Texas Health Science Center at San Antonio, San Antonio, Texas, USA
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Abstract

Here we review recent research into the mechanisms of chronic pain that has focused on neuronal sodium channels, a target of classic analgesic agents. We first discuss evidence that specific sodium channel isoforms are essential for the detection and conduction of normal acutely painful stimuli from nociceptors. We then review findings that show changes in sodium channel expression and localization in chronic inflammation and nerve injury in animal and human tissues. We conclude by discussing the role that myelination plays in organizing and maintaining sodium channel clusters at nodes of Ranvier in normal development and how inflammatory processes or nerve injury alter the characteristics of such clusters. Based on these findings, we suggest that chronic pain may in part result from partial demyelination of axons during chronic injury, which creates aberrant sodium channel clusters that serve as sites of ectopic sensitivity or spontaneous activity. Muscle Nerve 46: 155–165, 2012

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