Inflammatory mediators increase Nav1.9 current and excitability in nociceptors through a coincident detection mechanism.
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A de novo gain-of-function mutation in SCN11A causes loss of pain perceptionNeurotransmitter modulation of small-conductance Ca2+-activated K+ channels by regulation of Ca2+ gatingThe acute nociceptive signals induced by bradykinin in rat sensory neurons are mediated by inhibition of M-type K+ channels and activation of Ca2+-activated Cl- channels.Nav1.9 channel contributes to mechanical and heat pain hypersensitivity induced by subacute and chronic inflammation.Positive allosteric modulation of TRPV1 as a novel analgesic mechanism.Insensitivity to pain induced by a potent selective closed-state Nav1.7 inhibitor.Correlation of Nav1.8 and Nav1.9 sodium channel expression with neuropathic pain in human subjects with lingual nerve neuromas.Ionic mechanisms underlying inflammatory mediator-induced sensitization of dural afferents.Multiple roles for NaV1.9 in the activation of visceral afferents by noxious inflammatory, mechanical, and human disease-derived stimuli.Functional properties and toxin pharmacology of a dorsal root ganglion sodium channel viewed through its voltage sensorsIdentification and bioactivity evaluation of a novel bradykinin inhibitory peptide from the skin secretion of Chinese large odorous frog, Odorrana livida.Enhanced excitability of small dorsal root ganglion neurons in rats with bone cancer pain.Biophysical and Pharmacological Characterization of Nav1.9 Voltage Dependent Sodium Channels Stably Expressed in HEK-293 Cells.Animal toxins can alter the function of Nav1.8 and Nav1.9.Post-translational modifications of voltage-gated sodium channels in chronic pain syndromesMechanism of sodium channel NaV1.9 potentiation by G-protein signalingThe Nav1.9 channel regulates colonic motility in mice.Effect of amitriptyline on tetrodotoxin-resistant Nav1.9 currents in nociceptive trigeminal neurons.Characterization of persistent TTX-R Na+ currents in physiological concentration of sodium in rat visceral afferents.Nociceptors are interleukin-1beta sensorsElectrophysiological properties of dural afferents in the absence and presence of inflammatory mediators.Gain-of-function mutations in SCN11A cause familial episodic pain.Potassium channels in peripheral pain pathways: expression, function and therapeutic potential.Antinociceptive Effects of AGAP, a Recombinant Neurotoxic Polypeptide: Possible Involvement of the Tetrodotoxin-Resistant Sodium Channels in Small Dorsal Root Ganglia Neurons.Anoctamin 1 contributes to inflammatory and nerve-injury induced hypersensitivity.Transduction and encoding sensory information by skin mechanoreceptors.New insights of nociceptor sensitization in bone cancer pain.The voltage-gated sodium channel NaV 1.9 in visceral pain.Gain-of-function mutation p.Arg225Cys in SCN11A causes familial episodic pain and contributes to essential tremor.The role of slow and persistent TTX-resistant sodium currents in acute tumor necrosis factor-α-mediated increase in nociceptors excitability.C-fiber recovery cycle supernormality depends on ion concentration and ion channel permeability.Stromal Cell-Derived Factor 1 Increases Tetrodotoxin-Resistant Sodium Currents Nav1.8 and Nav1.9 in Rat Dorsal Root Ganglion Neurons via Different Mechanisms.Modeling activity-dependent changes of axonal spike conduction in primary afferent C-nociceptors.Ciguatoxins Evoke Potent CGRP Release by Activation of Voltage-Gated Sodium Channel Subtypes NaV1.9, NaV1.7 and NaV1.1.The Role of Kv7/M Potassium Channels in Controlling Ectopic Firing in Nociceptors.Na(+) current expression in human atrial myofibroblasts: identity and functional roles.Targeting voltage-gated sodium channels for treatment for chronic visceral pain.The role of Nav1.9 channel in the development of neuropathic orofacial pain associated with trigeminal neuralgia.Activation of neurokinin 3 receptor increases Na(v)1.9 current in enteric neurons.Morphological and functional changes in guinea-pig neurons projecting to the ileal mucosa at early stages after inflammatory damage.
P2860
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P2860
Inflammatory mediators increase Nav1.9 current and excitability in nociceptors through a coincident detection mechanism.
description
2008 nî lūn-bûn
@nan
2008年の論文
@ja
2008年学术文章
@wuu
2008年学术文章
@zh-cn
2008年学术文章
@zh-hans
2008年学术文章
@zh-my
2008年学术文章
@zh-sg
2008年學術文章
@yue
2008年學術文章
@zh
2008年學術文章
@zh-hant
name
Inflammatory mediators increas ...... oincident detection mechanism.
@ast
Inflammatory mediators increas ...... oincident detection mechanism.
@en
type
label
Inflammatory mediators increas ...... oincident detection mechanism.
@ast
Inflammatory mediators increas ...... oincident detection mechanism.
@en
prefLabel
Inflammatory mediators increas ...... oincident detection mechanism.
@ast
Inflammatory mediators increas ...... oincident detection mechanism.
@en
P2093
P2860
P356
P1476
Inflammatory mediators increas ...... oincident detection mechanism.
@en
P2093
Bertrand Coste
François Maingret
Françoise Padilla
Marcel Crest
Nadine Clerc
Patrick Delmas
Sergiy M Korogod
P2860
P304
P356
10.1085/JGP.200709935
P577
2008-02-11T00:00:00Z