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Sensory neuron sodium channel Nav1.8 is essential for pain at low temperatures

Author

Listed:
  • Katharina Zimmermann

    (Department of Physiology and Pathophysiology,)

  • Andreas Leffler

    (Faculty of Medicine, Friedrich-Alexander University Erlangen-Nuremberg, 91054 Erlangen, Germany)

  • Alexandru Babes

    (Department of Physiology and Pathophysiology,
    Faculty of Biology, University of Bucharest, 050095 Bucharest, Romania)

  • Cruz Miguel Cendan

    (University College London, London WC1E 6BT, UK)

  • Richard W. Carr

    (Department of Physiology and Pathophysiology,)

  • Jin-ichi Kobayashi

    (Faculty of Dental Science, Kyushu University, Maidashi 3-1-1, Higashi-ku, Fukuoka 812-8582, Japan)

  • Carla Nau

    (Faculty of Medicine, Friedrich-Alexander University Erlangen-Nuremberg, 91054 Erlangen, Germany)

  • John N. Wood

    (University College London, London WC1E 6BT, UK)

  • Peter W. Reeh

    (Department of Physiology and Pathophysiology,)

Abstract

Sensory acuity deteriorates at cold temperatures, but pain perception persists and cold stimuli themselves can be painful. A voltage-gated sodium channel, Nav1.8, is implicated in this perception. Unlike other channels, Nav1.8 does not inactivate at lower temperatures and its currents are actually larger in colder conditions

Suggested Citation

  • Katharina Zimmermann & Andreas Leffler & Alexandru Babes & Cruz Miguel Cendan & Richard W. Carr & Jin-ichi Kobayashi & Carla Nau & John N. Wood & Peter W. Reeh, 2007. "Sensory neuron sodium channel Nav1.8 is essential for pain at low temperatures," Nature, Nature, vol. 447(7146), pages 856-859, June.
    • Handle: RePEc:nat:nature:v:447:y:2007:i:7146:d:10.1038_nature05880
    DOI: 10.1038/nature05880
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    Cited by:

    1. Bryan Neumann & Stephen McCarthy & Shane Gonen, 2025. "Structural basis of inhibition of human NaV1.8 by the tarantula venom peptide Protoxin-I," Nature Communications, Nature, vol. 16(1), pages 1-10, December.

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