Journal
CELL REPORTS
Volume 11, Issue 7, Pages 1067-1078Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2015.04.027
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Funding
- Agence Nationale de la Recherche [ANR-08-MNPS-025-02, ANR-09-MNPS-037-01]
- Fondation pour la Recherche Medicale [FRM 2013 DEQ20130326482]
- ARC/INCa
- CNRS
- INSERM
- Aix-Marseille Universite
- Fondation pour la Recherche Medicale
- Ministere de l'Enseignement Superieur et de la Recherche
- La Ligue contre le cancer
- Universite d'Auvergne
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Cold-triggered pain is essential to avoid prolonged exposure to harmfully low temperatures. However, the molecular basis of noxious cold sensing in mammals is still not completely understood. Here, we show that the voltage-gated Nav1.9 sodium channel is important for the perception of pain in response to noxious cold. Nav1.9 activity is upregulated in a subpopulation of damage-sensing sensory neurons responding to cooling, which allows the channel to amplify subthreshold depolarizations generated by the activation of cold transducers. Consequently, cold-triggered firing is impaired in Nav1.9(-/-) neurons, and Nav1.9 null mice and knockdown rats show increased cold pain thresholds. Disrupting Nav1.9 expression in rodents also alleviates cold pain hypersensitivity induced by the antineoplastic agent oxaliplatin. We conclude that Nav1.9 acts as a subthreshold amplifier in cold-sensitive nociceptive neurons and is required for the perception of cold pain under normal and pathological conditions.
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