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Distinct Nav1.7-dependent pain sensations require different sets of sensory and sympathetic neurons

Author

Listed:
  • Michael S. Minett

    (Molecular Nociception Group, WIBR UCL)

  • Mohammed A. Nassar

    (The University of Sheffield)

  • Anna K. Clark

    (Wolfson Centre for Age-Related Diseases, King's College London, Guy's Campus)

  • Gayle Passmore

    (Molecular Nociception Group, WIBR UCL)

  • Anthony H. Dickenson

    (University College London)

  • Fan Wang

    (Duke University Medical Center)

  • Marzia Malcangio

    (Wolfson Centre for Age-Related Diseases, King's College London, Guy's Campus)

  • John N. Wood

    (Molecular Nociception Group, WIBR UCL)

Abstract

Human acute and inflammatory pain requires the expression of voltage-gated sodium channel Nav1.7 but its significance for neuropathic pain is unknown. Here we show that Nav1.7 expression in different sets of mouse sensory and sympathetic neurons underlies distinct types of pain sensation. Ablating Nav1.7 gene (SCN9A) expression in all sensory neurons using Advillin-Cre abolishes mechanical pain, inflammatory pain and reflex withdrawal responses to heat. In contrast, heat-evoked pain is retained when SCN9A is deleted only in Nav1.8-positive nociceptors. Surprisingly, responses to the hotplate test, as well as neuropathic pain, are unaffected when SCN9A is deleted in all sensory neurons. However, deleting SCN9A in both sensory and sympathetic neurons abolishes these pain sensations and recapitulates the pain-free phenotype seen in humans with SCN9A loss-of-function mutations. These observations demonstrate an important role for Nav1.7 in sympathetic neurons in neuropathic pain, and provide possible insights into the mechanisms that underlie gain-of-function Nav1.7-dependent pain conditions.

Suggested Citation

  • Michael S. Minett & Mohammed A. Nassar & Anna K. Clark & Gayle Passmore & Anthony H. Dickenson & Fan Wang & Marzia Malcangio & John N. Wood, 2012. "Distinct Nav1.7-dependent pain sensations require different sets of sensory and sympathetic neurons," Nature Communications, Nature, vol. 3(1), pages 1-9, January.
    • Handle: RePEc:nat:natcom:v:3:y:2012:i:1:d:10.1038_ncomms1795
    DOI: 10.1038/ncomms1795
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    Cited by:

    1. Sina Jami & Jennifer R. Deuis & Tabea Klasfauseweh & Xiaoyang Cheng & Sergey Kurdyukov & Felicity Chung & Andrei L. Okorokov & Shengnan Li & Jiangtao Zhang & Ben Cristofori-Armstrong & Mathilde R. Isr, 2023. "Pain-causing stinging nettle toxins target TMEM233 to modulate NaV1.7 function," Nature Communications, Nature, vol. 14(1), pages 1-16, December.

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