Sodium channels and mammalian sensory mechanotransduction.

Détails

Ressource 1Télécharger: BIB_4AC071086618.P001.pdf (940.55 [Ko])
Etat: Public
Version: de l'auteur
ID Serval
serval:BIB_4AC071086618
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Sodium channels and mammalian sensory mechanotransduction.
Périodique
Molecular Pain
Auteur(s)
Raouf R., Rugiero F., Kiesewetter H., Hatch R., Hummler E., Nassar M.A., Wang F., Wood J.N.
ISSN
1744-8069 (Electronic)
ISSN-L
1744-8069
Statut éditorial
Publié
Date de publication
03/2012
Peer-reviewed
Oui
Volume
8
Numéro
1
Pages
21
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: epublish
Résumé
BACKGROUND: Members of the degenerin/epithelial (DEG/ENaC) sodium channel family are mechanosensors in C elegans, and Nav1.7 and Nav1.8 voltage-gated sodium channel knockout mice have major deficits in mechanosensation. β and γENaC sodium channel subunits are present with acid sensing ion channels (ASICs) in mammalian sensory neurons of the dorsal root ganglia (DRG). The extent to which epithelial or voltage-gated sodium channels are involved in transduction of mechanical stimuli is unclear.
RESULTS: Here we show that deleting β and γENaC sodium channels in sensory neurons does not result in mechanosensory behavioural deficits. We had shown previously that Nav1.7/Nav1.8 double knockout mice have major deficits in behavioural responses to noxious mechanical pressure. However, all classes of mechanically activated currents in DRG neurons are unaffected by deletion of the two sodium channels. In contrast, the ability of Nav1.7/Nav1.8 knockout DRG neurons to generate action potentials is compromised with 50% of the small diameter sensory neurons unable to respond to electrical stimulation in vitro.
CONCLUSION: Behavioural deficits in Nav1.7/Nav1.8 knockout mice reflects a failure of action potential propagation in a mechanosensitive set of sensory neurons rather than a loss of primary transduction currents. DEG/ENaC sodium channels are not mechanosensors in mouse sensory neurons.
Mots-clé
Action Potentials/genetics, Action Potentials/physiology, Animals, Epithelial Sodium Channels/genetics, Epithelial Sodium Channels/metabolism, Mechanotransduction, Cellular/genetics, Mechanotransduction, Cellular/physiology, Mice, Mice, Knockout, NAV1.7 Voltage-Gated Sodium Channel, NAV1.8 Voltage-Gated Sodium Channel, Sensory Receptor Cells/metabolism, Sodium Channels/genetics, Sodium Channels/metabolism
Pubmed
Web of science
Open Access
Oui
Création de la notice
28/06/2012 18:57
Dernière modification de la notice
20/08/2019 14:58
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