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

Katharina Zimmermann (), Andreas Leffler, Alexandru Babes, Cruz Miguel Cendan, Richard W. Carr, Jin-ichi Kobayashi, Carla Nau, John N. Wood and Peter W. Reeh
Additional contact information
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,
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,

Nature, 2007, vol. 447, issue 7146, 856-859

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

Date: 2007
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DOI: 10.1038/nature05880

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