Slow closed-state inactivation: a novel mechanism underlying ramp currents in cells expressing the hNE/PN1 sodium channel.
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Association between tetrodotoxin resistant channels and lipid rafts regulates sensory neuron excitabilityTemperature dependence of erythromelalgia mutation L858F in sodium channel Nav1.7Characterization of a de novo SCN8A mutation in a patient with epileptic encephalopathyA single sodium channel mutation produces hyper- or hypoexcitability in different types of neuronsA Nav1.7 channel mutation associated with hereditary erythromelalgia contributes to neuronal hyperexcitability and displays reduced lidocaine sensitivityConotoxins That Could Provide Analgesia through Voltage Gated Sodium Channel InhibitionPrimary erythromelalgia: a reviewCellular hyper-excitability caused by mutations that alter the activation process of voltage-gated sodium channelsThe perception and endogenous modulation of painRoles of Voltage-Gated Tetrodotoxin-Sensitive Sodium Channels NaV1.3 and NaV1.7 in Diabetes and Painful Diabetic NeuropathySodium currents of large (Abeta-type) adult cutaneous afferent dorsal root ganglion neurons display rapid recovery from inactivation before and after axotomyGlobal Nav1.7 knockout mice recapitulate the phenotype of human congenital indifference to painSubtype-Selective Small Molecule Inhibitors Reveal a Fundamental Role for Nav1.7 in Nociceptor Electrogenesis, Axonal Conduction and Presynaptic Release.Splice variants of Na(V)1.7 sodium channels have distinct β subunit-dependent biophysical propertiesOtotrauma induces sodium channel plasticity in auditory afferent neuronsPharmacological characterisation of the highly NaV1.7 selective spider venom peptide Pn3a.Multiple sodium channel isoforms mediate the pathological effects of Pacific ciguatoxin-1.Voltage-gated sodium channels in taste bud cells.Sodium channel Na v 1.7 immunoreactivity in painful human dental pulp and burning mouth syndrome.Sodium channels and pain.Voltage-gated Na+ currents in human dorsal root ganglion neurons.Pain perception is altered by a nucleotide polymorphism in SCN9AAlternative splicing of Na(V)1.7 exon 5 increases the impact of the painful PEPD mutant channel I1461T.The neuron as a dynamic electrogenic machine: modulation of sodium-channel expression as a basis for functional plasticity in neurons.Mutations at opposite ends of the DIII/S4-S5 linker of sodium channel Na V 1.7 produce distinct pain disordersBlockade of persistent sodium currents contributes to the riluzole-induced inhibition of spontaneous activity and oscillations in injured DRG neurons.A novel Nav1.7 mutation producing carbamazepine-responsive erythromelalgia.A nonsense mutation in the SCN9A gene in congenital insensitivity to painGain-of-function Nav1.8 mutations in painful neuropathy.mTORC1 inhibition induces pain via IRS-1-dependent feedback activation of ERK.A novel SCN9A mutation responsible for primary erythromelalgia and is resistant to the treatment of sodium channel blockersMutations in sodium-channel gene SCN9A cause a spectrum of human genetic pain disorders.Are voltage-gated sodium channels on the dorsal root ganglion involved in the development of neuropathic pain?The roles of sodium channels in nociception: Implications for mechanisms of painMolecular and functional remodeling of electrogenic membrane of hypothalamic neurons in response to changes in their inputNav1.7 is the predominant sodium channel in rodent olfactory sensory neurons.Human Na(v)1.8: enhanced persistent and ramp currents contribute to distinct firing properties of human DRG neurons.Intra- and interfamily phenotypic diversity in pain syndromes associated with a gain-of-function variant of NaV1.7.Early painful diabetic neuropathy is associated with differential changes in tetrodotoxin-sensitive and -resistant sodium channels in dorsal root ganglion neurons in the rat.Human Nav1.6 Channels Generate Larger Resurgent Currents than Human Nav1.1 Channels, but the Navβ4 Peptide Does Not Protect Either Isoform from Use-Dependent Reduction.
P2860
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P2860
Slow closed-state inactivation: a novel mechanism underlying ramp currents in cells expressing the hNE/PN1 sodium channel.
description
1998 nî lūn-bûn
@nan
1998年の論文
@ja
1998年論文
@yue
1998年論文
@zh-hant
1998年論文
@zh-hk
1998年論文
@zh-mo
1998年論文
@zh-tw
1998年论文
@wuu
1998年论文
@zh
1998年论文
@zh-cn
name
Slow closed-state inactivation ...... ng the hNE/PN1 sodium channel.
@en
Slow closed-state inactivation ...... ng the hNE/PN1 sodium channel.
@nl
type
label
Slow closed-state inactivation ...... ng the hNE/PN1 sodium channel.
@en
Slow closed-state inactivation ...... ng the hNE/PN1 sodium channel.
@nl
prefLabel
Slow closed-state inactivation ...... ng the hNE/PN1 sodium channel.
@en
Slow closed-state inactivation ...... ng the hNE/PN1 sodium channel.
@nl
P2093
P1476
Slow closed-state inactivation ...... ing the hNE/PN1 sodium channel
@en
P2093
P304
P356
10.1523/JNEUROSCI.18-23-09607.1998
P407
P577
1998-12-01T00:00:00Z