ArticlePflugers Archiv : European journal of physiology2004
Electrophysiological characterization of the tetrodotoxin-resistant Na+ channel, Na(v)1.9, in mouse dorsal root ganglion neurons.
Article in Pflugers Archiv : European journal of physiology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed.
- Infantile Pain Episodes Associated with Novel Nav1.9 Mutations in Familial Episodic Pain Syndrome in Japanese Families.PloS one · 2016Trial
- Modulation of Voltage-Gated Sodium Channels from Sensory Neurons by Isoeugenol.International journal of molecular sciences · 2025Article
- A robust expression system reveals distinct gating mechanisms and calmodulin regulation of NaScience advances · 2025Article
- State-Dependent Blockade of Dorsal Root Ganglion Voltage-Gated NaInternational journal of molecular sciences · 2024Article
- Eugenol and lidocaine inhibit voltage-gated NaFrontiers in pharmacology · 2024Article
- Painful and painless mutations of SCN9A and SCN11A voltage-gated sodium channels.Pflugers Archiv : European journal of physiology · 2020Review
- A disease mutation reveals a role for NaV1.9 in acute itch.The Journal of clinical investigation · 2018Article
- NaJournal of neurophysiology · 2018Article
- Hierarchical CRMP2 posttranslational modifications control NaV1.7 function.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Gi-DREADD Expression in Peripheral Nerves Produces Ligand-Dependent Analgesia, as well as Ligand-Independent Functional Changes in Sensory Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- The role of Nav1.9 channel in the development of neuropathic orofacial pain associated with trigeminal neuralgia.Molecular pain · 2015Article
- NaV1.9: a sodium channel linked to human pain.Nature reviews. Neuroscience · 2015Review
- CC chemokine ligand 2 upregulates the current density and expression of TRPV1 channels and Nav1.8 sodium channels in dorsal root ganglion neurons.Journal of neuroinflammation · 2012Article
- Review
- Functional properties and toxin pharmacology of a dorsal root ganglion sodium channel viewed through its voltage sensors.The Journal of general physiology · 2011Article
- Regulation of the spontaneous augmentation of Na(V)1.9 in mouse dorsal root ganglion neurons: effect of PKA and PKC pathways.Marine drugs · 2010Article
- Functional neurons and melanocytes induced from immortal lines of postnatal neural crest-like stem cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2009Article
- Non-invasive imaging of stem cells by scanning ion conductance microscopy: future perspective.Tissue engineering. Part C, Methods · 2008Article
- The chemokine CXCL1/growth related oncogene increases sodium currents and neuronal excitability in small diameter sensory neurons.Molecular pain · 2008Article
- Inflammatory mediators increase Nav1.9 current and excitability in nociceptors through a coincident detection mechanism.The Journal of general physiology · 2008Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Small dorsal root ganglion neurons express preferentially the Na+ channel isoform Na(v)1.9 that mediates a tetrodotoxin-resistant (TTX-R) Na+ current. We investigated properties of the Na+ current mediated by Na(v)1.9 (I(NaN)) using the whole-cell, patch-clamp recording technique. To isolate I(NaN) from heterogeneous TTX-R Na+ currents that also contain another type of TTX-R Na+ current mediated by Na(v)1.8, we used Na(v)1.8-null mutant mice. When F- was used as an internal anion in the patch pipette solution, both the activation and inactivation kinetics for I(NaN) shifted in the hyperpolarizing direction with time. Such a time-dependent shift of the kinetics was not observed when Cl- was used as an internal anion. Functional expression of I(NaN) declined with time after cell dissociation and recovered during culture, implying that Na(v)1.9 may be regulated dynamically by trophic factors or depend on subtle environmental factors for its survival. During whole-cell recordings, the peak amplitude of I(NaN) increased dramatically after a variable delay, as if inactive or silent channels had been "kindled". Such an unusual increase of the amplitude could be prevented by adding ATP to the pipette solution or by recording with the nystatin-perforated patch-clamp technique, suggesting that the rupture of patch membrane affected the behaviour of Na(v)1.9. These peculiar properties of I(NaN) may provide an insight into the plasticity of Na+ channels that are related to pathological functions of Na+ channels accompanying abnormal pain states.
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Registered trials
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