Na(v)1.5 underlies the 'third TTX-R sodium current' in rat small DRG neurons.
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Modulation of the cardiac sodium channel Nav1.5 by fibroblast growth factor homologous factor 1BMolecular profiling of murine sensory neurons in the nodose and dorsal root ganglia labeled from the peritoneal cavity.Multiple Nav1.5 isoforms are functionally expressed in the brain and present distinct expression patterns compared with cardiac Nav1.5.An in vivo tethered toxin approach for the cell-autonomous inactivation of voltage-gated sodium channel currents in nociceptors.The roles of sodium channels in nociception: Implications for mechanisms of painModeling pain in vitro using nociceptor neurons reprogrammed from fibroblasts.Ion channels in mammalian vestibular afferents may set regularity of firing.Functional expression of "cardiac-type" Nav1.5 sodium channel in canine intracardiac ganglia.Inhibition of voltage-gated Na(+) currents in sensory neurones by the sea anemone toxin APETx2.Post-translational modifications of voltage-gated sodium channels in chronic pain syndromesBlocking sodium channels to treat neuropathic pain.Voltage-gated sodium channel blockers for the treatment of neuropathic pain.Sodium channel diversity in the vestibular ganglion: NaV1.5, NaV1.8, and tetrodotoxin-sensitive currents.The sodium channel Nav1.5a is the predominant isoform expressed in adult mouse dorsal root ganglia and exhibits distinct inactivation properties from the full-length Nav1.5 channel.Novel isoforms of the sodium channels Nav1.8 and Nav1.5 are produced by a conserved mechanism in mouse and rat.Exploring the obscure profiles of pharmacological binding sites on voltage-gated sodium channels by BmK neurotoxins.Sodium Channel Nav1.8 Underlies TTX-Resistant Axonal Action Potential Conduction in Somatosensory C-Fibers of Distal Cutaneous Nerves.Pattern of Functional TTX-Resistant Sodium Channels Reveals a Developmental Stage of Human iPSC- and ESC-Derived NociceptorsVisceral and somatic pain modalities reveal NaV 1.7-independent visceral nociceptive pathways.Increased peripheral nerve excitability and local NaV1.8 mRNA up-regulation in painful neuropathy.Low concentrations of tetrodotoxin interact with tetrodotoxin-resistant voltage-gated sodium channels.Two TTX-resistant Na+ currents in mouse colonic dorsal root ganglia neurons and their role in colitis-induced hyperexcitability.Pyramidal cells of rodent presubiculum express a tetrodotoxin-insensitive Na+ current.Voltage-gated sodium channels in nociceptive versus non-nociceptive nodose vagal sensory neurons innervating guinea pig lungs.Membrane properties and electrogenesis in the distal axons of small dorsal root ganglion neurons in vitro.Properties of wild-type and fluorescent protein-tagged mouse tetrodotoxin-resistant sodium channel (Na V 1.8) heterologously expressed in rat sympathetic neurons.Lidocaine promotes the trafficking and functional expression of Na(v)1.8 sodium channels in mammalian cells.Developmental changes in two voltage-dependent sodium currents in utricular hair cells.The TTX-resistant sodium channel Nav1.8 (SNS/PN3): expression and correlation with membrane properties in rat nociceptive primary afferent neurons.Differential slow inactivation and use-dependent inhibition of Nav1.8 channels contribute to distinct firing properties in IB4+ and IB4- DRG neurons.Development and validation of an in vitro model system to study peripheral sensory neuron development and injury
P2860
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P2860
Na(v)1.5 underlies the 'third TTX-R sodium current' in rat small DRG neurons.
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2002 nî lūn-bûn
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name
Na(v)1.5 underlies the 'third TTX-R sodium current' in rat small DRG neurons.
@en
type
label
Na(v)1.5 underlies the 'third TTX-R sodium current' in rat small DRG neurons.
@en
prefLabel
Na(v)1.5 underlies the 'third TTX-R sodium current' in rat small DRG neurons.
@en
P2093
P1476
Na(v)1.5 underlies the 'third TTX-R sodium current' in rat small DRG neurons.
@en
P2093
Dib-Hajj S
Renganathan M
P356
10.1016/S0169-328X(02)00411-4
P577
2002-10-01T00:00:00Z