A novel persistent tetrodotoxin-resistant sodium current in SNS-null and wild-type small primary sensory neurons
about
A Nav1.7 channel mutation associated with hereditary erythromelalgia contributes to neuronal hyperexcitability and displays reduced lidocaine sensitivitySodium currents of large (Abeta-type) adult cutaneous afferent dorsal root ganglion neurons display rapid recovery from inactivation before and after axotomyThe chemokine CXCL1/growth related oncogene increases sodium currents and neuronal excitability in small diameter sensory neuronsVoltage-gated sodium channel in grasshopper mice defends against bark scorpion toxinToxin-resistant sodium channels: parallel adaptive evolution across a complete gene family.Functional neurons and melanocytes induced from immortal lines of postnatal neural crest-like stem cells.Nav1.9 channel contributes to mechanical and heat pain hypersensitivity induced by subacute and chronic inflammation.Correlation of Nav1.8 and Nav1.9 sodium channel expression with neuropathic pain in human subjects with lingual nerve neuromas.Burning pain: axonal dysfunction in erythromelalgia.Tetrodotoxin-resistant sodium channels in sensory neurons generate slow resurgent currents that are enhanced by inflammatory mediators.Identifying the Ion Channels Responsible for Signaling Gastro-Intestinal Based PainContribution of the tetrodotoxin-resistant voltage-gated sodium channel NaV1.9 to sensory transmission and nociceptive behavior.Antisense-mediated knockdown of Na(V)1.8, but not Na(V)1.9, generates inhibitory effects on complete Freund's adjuvant-induced inflammatory pain in rat.An in vivo tethered toxin approach for the cell-autonomous inactivation of voltage-gated sodium channel currents in nociceptors.PKCε phosphorylation of the sodium channel NaV1.8 increases channel function and produces mechanical hyperalgesia in mice.Modulation of neuronal sodium channels by the sea anemone peptide BDS-I.Dysregulation of voltage-gated sodium channels by ubiquitin ligase NEDD4-2 in neuropathic pain.Single-cell analysis of sodium channel expression in dorsal root ganglion neuronsInhibition of tetrodotoxin-resistant sodium current in dorsal root ganglia neurons mediated by D1/D5 dopamine receptorsA-803467, a potent and selective Nav1.8 sodium channel blocker, attenuates neuropathic and inflammatory pain in the rat.The roles of sodium channels in nociception: Implications for mechanisms of painExpansion of voltage-dependent Na+ channel gene family in early tetrapods coincided with the emergence of terrestriality and increased brain complexityFunctional properties and toxin pharmacology of a dorsal root ganglion sodium channel viewed through its voltage sensorsSensory neuron-specific sodium channel SNS is abnormally expressed in the brains of mice with experimental allergic encephalomyelitis and humans with multiple sclerosisCharacteristics of sodium currents in rat geniculate ganglion neuronsHuman Na(v)1.8: enhanced persistent and ramp currents contribute to distinct firing properties of human DRG neurons.Inactivation properties of sodium channel Nav1.8 maintain action potential amplitude in small DRG neurons in the context of depolarization.Local inflammation in rat dorsal root ganglion alters excitability and ion currents in small-diameter sensory neurons.A novel substituted aminoquinoline selectively targets voltage-sensitive sodium channel isoforms and NMDA receptor subtypes and alleviates chronic inflammatory and neuropathic pain.Navβ4 regulates fast resurgent sodium currents and excitability in sensory neuronsBiophysical and Pharmacological Characterization of Nav1.9 Voltage Dependent Sodium Channels Stably Expressed in HEK-293 Cells.Inhibition of voltage-gated Na(+) currents in sensory neurones by the sea anemone toxin APETx2.Animal toxins can alter the function of Nav1.8 and Nav1.9.Pharmacological dissection and distribution of NaN/Nav1.9, T-type Ca2+ currents, and mechanically activated cation currents in different populations of DRG neurons.Cold-aggravated pain in humans caused by a hyperactive NaV1.9 channel mutant.Conotoxins targeting neuronal voltage-gated sodium channel subtypes: potential analgesics?The effects of polarizing current on nerve terminal impulses recorded from polymodal and cold receptors in the guinea-pig cornea.Inflammatory mediators increase Nav1.9 current and excitability in nociceptors through a coincident detection mechanism.Mutation I136V alters electrophysiological properties of the Na(v)1.7 channel in a family with onset of erythromelalgia in the second decadeElectrophysiological characterization of Grueneberg ganglion olfactory neurons: spontaneous firing, sodium conductance, and hyperpolarization-activated currents.
P2860
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P2860
A novel persistent tetrodotoxin-resistant sodium current in SNS-null and wild-type small primary sensory neurons
description
1999 nî lūn-bûn
@nan
1999 թուականի Դեկտեմբերին հրատարակուած գիտական յօդուած
@hyw
1999 թվականի դեկտեմբերին հրատարակված գիտական հոդված
@hy
1999年の論文
@ja
1999年論文
@yue
1999年論文
@zh-hant
1999年論文
@zh-hk
1999年論文
@zh-mo
1999年論文
@zh-tw
1999年论文
@wuu
name
A novel persistent tetrodotoxi ...... small primary sensory neurons
@ast
A novel persistent tetrodotoxi ...... small primary sensory neurons
@en
A novel persistent tetrodotoxi ...... small primary sensory neurons
@nl
type
label
A novel persistent tetrodotoxi ...... small primary sensory neurons
@ast
A novel persistent tetrodotoxi ...... small primary sensory neurons
@en
A novel persistent tetrodotoxi ...... small primary sensory neurons
@nl
prefLabel
A novel persistent tetrodotoxi ...... small primary sensory neurons
@ast
A novel persistent tetrodotoxi ...... small primary sensory neurons
@en
A novel persistent tetrodotoxi ...... small primary sensory neurons
@nl
P2093
P1476
A novel persistent tetrodotoxi ...... small primary sensory neurons
@en
P2093
A N Akopian
S D Dib-Hajj
S G Waxman
T R Cummins
P407
P577
1999-12-15T00:00:00Z