ArticleMolecular pain2012
Sodium channels and mammalian sensory mechanotransduction.
Article in Molecular pain, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 25 citations in OpenAlex.
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- Mechanical Strain-Mediated Tenogenic Differentiation of Mesenchymal Stromal Cells Is Regulated through Epithelial Sodium Channels.Stem cells international · 2020Article
- Defining the Functional Role of NaNeuron · 2019Article
- Pore-lining residues of MEC-4 and MEC-10 channel subunits tune theThe Journal of biological chemistry · 2018Article
- Analgesia linked to Nav1.7 loss of function requires µ- and δ-opioid receptors.Wellcome open research · 2018Article
- The function and regulation of acid-sensing ion channels (ASICs) and the epithelial Na(+) channel (ENaC): IUPHAR Review 19.British journal of pharmacology · 2016Review
- Merkel Cell-Driven BDNF Signaling Specifies SAI Neuron Molecular and Electrophysiological Phenotypes.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Endogenous opioids contribute to insensitivity to pain in humans and mice lacking sodium channel Nav1.7.Nature communications · 2015Article
- Regulation of alternative VEGF-A mRNA splicing is a therapeutic target for analgesia.Neurobiology of disease · 2014Article
- Null mutation in SCN9A in which noxious stimuli can be detected in the absence of pain.Neurology · 2014Article
- Carbamazepine potentiates the effectiveness of morphine in a rodent model of neuropathic pain.PloS one · 2014Article
- Towards a mechanism-based approach to pain management in osteoarthritis.Nature reviews. Rheumatology · 2013Review
- Distinct Nav1.7-dependent pain sensations require different sets of sensory and sympathetic neurons.Nature communications · 2012Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 4 countries.
Funding
Abstract
backgroundMembers 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.
resultsHere 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.
conclusionBehavioural 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.
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