A-803467, a potent and selective Nav1.8 sodium channel blocker, attenuates neuropathic and inflammatory pain in the rat. - Wikidata - awgldk - TriplyDB

A-803467, a potent and selective Nav1.8 sodium channel blocker, attenuates neuropathic and inflammatory pain in the rat.

A-803467, a potent and selective Nav1.8 sodium channel blocker, attenuates neuropathic and inflammatory pain in the rat.

http://www.wikidata.org/entity/Q34625901

about

Association between tetrodotoxin resistant channels and lipid rafts regulates sensory neuron excitability Structural determinants of drugs acting on the Nav1.8 channel Synthetic ciguatoxins selectively activate Nav1.8-derived chimeric sodium channels expressed in HEK293 cells The role of visceral hypersensitivity in irritable bowel syndrome: pharmacological targets and novel treatments Conotoxins That Could Provide Analgesia through Voltage Gated Sodium Channel Inhibition Structural Basis for Pharmacology of Voltage-Gated Sodium and Calcium Channels Modeling nociception in zebrafish: a way forward for unbiased analgesic discovery Relationship of axonal voltage-gated sodium channel 1.8 (NaV1.8) mRNA accumulation to sciatic nerve injury-induced painful neuropathy in rats Subtype-Selective Small Molecule Inhibitors Reveal a Fundamental Role for Nav1.7 in Nociceptor Electrogenesis, Axonal Conduction and Presynaptic Release.The 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.A gain-of-function voltage-gated sodium channel 1.8 mutation drives intense hyperexcitability of A- and C-fiber neurons.Experimental and computational evidence for an essential role of NaV1.6 in spike initiation at stretch-sensitive colorectal afferent endings Multiple sodium channel isoforms mediate the pathological effects of Pacific ciguatoxin-1.Blocking the Nav1.8 channel in the left stellate ganglion suppresses ventricular arrhythmia induced by acute ischemia in a canine model.Bilateral downregulation of Nav1.8 in dorsal root ganglia of rats with bone cancer pain induced by inoculation with Walker 256 breast tumor cells Targeting ASIC3 for Relieving Mice Fibromyalgia Pain: Roles of Electroacupuncture, Opioid, and Adenosine.Increase of sodium channels (nav 1.8 and nav 1.9) in rat dorsal root ganglion neurons exposed to autologous nucleus pulposus.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 Pain Voltage-gated Na+ currents in human dorsal root ganglion neurons.Roles of ASIC3, TRPV1, and NaV1.8 in the transition from acute to chronic pain in a mouse model of fibromyalgia.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.Intrathecal lidocaine pretreatment attenuates immediate neuropathic pain by modulating Nav1.3 expression and decreasing spinal microglial activation Regional differences in nerve terminal Na+ channel subtype expression and Na+ channel-dependent glutamate and GABA release in rat CNS.Additive antinociceptive effects of a combination of vitamin C and vitamin E after peripheral nerve injury.The trafficking of Na(V)1.8.Common variants in 22 loci are associated with QRS duration and cardiac ventricular conduction.Expression of 5-HT3 receptors and TTX resistant sodium channels (Na(V)1.8) on muscle nerve fibers in pain-free humans and patients with chronic myofascial temporomandibular disorders.Single-cell analysis of sodium channel expression in dorsal root ganglion neurons Ionic mechanisms of spinal neuronal cold hypersensitivity in ciguatera.Control of somatic membrane potential in nociceptive neurons and its implications for peripheral nociceptive transmission.Dorsal root tetrodotoxin-resistant sodium channels do not contribute to the augmented exercise pressor reflex in rats with chronic femoral artery occlusion.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 pain Functional upregulation of nav1.8 sodium channels on the membrane of dorsal root Ganglia neurons contributes to the development of cancer-induced bone pain Reporting sodium channel activity using calcium flux: pharmacological promiscuity of cardiac Nav1.5.Simplified bacterial "pore" channel provides insight into the assembly, stability, and structure of sodium channels.Probing functional properties of nociceptive axons using a microfluidic culture system.Dexmedetomidine inhibits Tetrodotoxin-resistant Nav1.8 sodium channel activity through Gi/o-dependent pathway in rat dorsal root ganglion neurons.

P2860

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P2860

A-803467, a potent and selective Nav1.8 sodium channel blocker, attenuates neuropathic and inflammatory pain in the rat.

http://www.wikidata.org/entity/Q34625901

description

2007 nî lūn-bûn

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2007 թուականի Մայիսին հրատարակուած գիտական յօդուած

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2007 թվականի մայիսին հրատարակված գիտական հոդված

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2007年の論文

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A-803467, a potent and selecti ...... inflammatory pain in the rat.

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A-803467, a potent and selecti ...... inflammatory pain in the rat.

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Proceedings of the National Academy of Sciences of the United States of America

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A-803467, a potent and selecti ...... inflammatory pain in the rat.

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Ahmed Hakeem

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Brian Marron

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Carrie Wade

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Chang Zhu

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Char-Chang Shieh

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Chengmin Zhong

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Connie R Faltynek

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Dong Liu

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Donna Gauvin

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Douglas S Krafte

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P2860

Overview of the voltage-gated sodium channel family

Neuropathic pain develops normally in mice lacking both Na(v)1.7 and Na(v)1.8.

A novel persistent tetrodotoxin-resistant sodium current in SNS-null and wild-type small primary sensory neurons

A comparison of the potential role of the tetrodotoxin-insensitive sodium channels, PN3/SNS and NaN/SNS2, in rat models of chronic pain.

Tetrodotoxin-resistant Na+ currents and inflammatory hyperalgesia

Sodium channels, excitability of primary sensory neurons, and the molecular basis of pain.

The tetrodotoxin-resistant sodium channel SNS has a specialized function in pain pathways.

Contribution of Na(v)1.8 sodium channels to action potential electrogenesis in DRG neurons.

Resurgence of sodium channel research.

Voltage-gated sodium channels and hyperalgesia.

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8520-8525

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neuropathic pain

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