Contribution of the tetrodotoxin-resistant voltage-gated sodium channel NaV1.9 to sensory transmission and nociceptive behavior. - Wikidata - wikimedia - TriplyDB

Contribution of the tetrodotoxin-resistant voltage-gated sodium channel NaV1.9 to sensory transmission and nociceptive behavior.

Contribution of the tetrodotoxin-resistant voltage-gated sodium channel NaV1.9 to sensory transmission and nociceptive behavior.

http://www.wikidata.org/entity/Q33878908

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Role of acid-sensing ion channel 3 in sub-acute-phase inflammation Conotoxins That Could Provide Analgesia through Voltage Gated Sodium Channel Inhibition Nav1.7 and other voltage-gated sodium channels as drug targets for pain relief A de novo gain-of-function mutation in SCN11A causes loss of pain perception Pain genes Global Nav1.7 knockout mice recapitulate the phenotype of human congenital indifference to pain Voltage-gated Na+ channels in neuropathic pain.Nav1.9 channel contributes to mechanical and heat pain hypersensitivity induced by subacute and chronic inflammation.Increase of sodium channels (nav 1.8 and nav 1.9) in rat dorsal root ganglion neurons exposed to autologous nucleus pulposus.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.Challenges in the development of novel treatment strategies for neuropathic pain.Role of Na(v)1.9 in activity-dependent axon growth in motoneurons.Single-cell analysis of sodium channel expression in dorsal root ganglion neurons Multiple roles for NaV1.9 in the activation of visceral afferents by noxious inflammatory, mechanical, and human disease-derived stimuli.Ion channelopathies in functional GI 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 pain Identification of genes concordantly expressed with Atoh1 during inner ear development.Na+ channel Scn1b gene regulates dorsal root ganglion nociceptor excitability in vivo Functional properties and toxin pharmacology of a dorsal root ganglion sodium channel viewed through its voltage sensors Nerve injury induces robust allodynia and ectopic discharges in Nav1.3 null mutant mice.Navβ subunits modulate the inhibition of Nav1.8 by the analgesic gating modifier μO-conotoxin MrVIB Dorsal root ganglion myeloid zinc finger protein 1 contributes to neuropathic pain after peripheral nerve trauma Inhibition of Navβ4 peptide-mediated resurgent sodium currents in Nav1.7 channels by carbamazepine, riluzole, and anandamide.The role of sodium channels in chronic pain.Animal toxins can alter the function of Nav1.8 and Nav1.9.Post-translational modifications of voltage-gated sodium channels in chronic pain syndromes Pharmacological dissection and distribution of NaN/Nav1.9, T-type Ca2+ currents, and mechanically activated cation currents in different populations of DRG neurons.Conotoxins targeting neuronal voltage-gated sodium channel subtypes: potential analgesics?Inflammatory mediators increase Nav1.9 current and excitability in nociceptors through a coincident detection mechanism.Mechanism of sodium channel NaV1.9 potentiation by G-protein signaling Voltage-gated sodium channels: action players with many faces.Cell-autonomous axon growth of young motoneurons is triggered by a voltage-gated sodium channel Multiple sodium channels and their roles in electrogenesis within dorsal root ganglion neurons.Differing alterations of sodium currents in small dorsal root ganglion neurons after ganglion compression and peripheral nerve injury.Blocking sodium channels to treat neuropathic pain.Electroacupuncture Reduces Carrageenan- and CFA-Induced Inflammatory Pain Accompanied by Changing the Expression of Nav1.7 and Nav1.8, rather than Nav1.9, in Mice Dorsal Root Ganglia The Nav1.9 channel regulates colonic motility in mice.Effect of amitriptyline on tetrodotoxin-resistant Nav1.9 currents in nociceptive trigeminal neurons.Voltage-gated sodium channel blockers for the treatment of neuropathic pain.

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Contribution of the tetrodotoxin-resistant voltage-gated sodium channel NaV1.9 to sensory transmission and nociceptive behavior.

http://www.wikidata.org/entity/Q33878908

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2005 nî lūn-bûn

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2005 թուականի Յունիսին հրատարակուած գիտական յօդուած

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2005 թվականի հունիսին հրատարակված գիտական հոդված

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2005年の論文

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Contribution of the tetrodotox ...... sion and nociceptive behavior.

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Contribution of the tetrodotox ...... sion and nociceptive behavior.

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Contribution of the tetrodotox ...... sion and nociceptive behavior.

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Contribution of the tetrodotox ...... sion and nociceptive behavior.

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Contribution of the tetrodotox ...... sion and nociceptive behavior.

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

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Contribution of the tetrodotox ...... sion and nociceptive behavior.

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Amy M Ritter

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Beth A Murphy

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Birgit T Priest

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Carmen Diaz

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Catherine Abbadie

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D Euan MacIntyre

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Gregory J Kaczorowski

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Jill A Lindia

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Leslie M Iyer

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Martin G Kohler

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P2860

Neurotrophin-evoked depolarization requires the sodium channel Na(V)1.9

Contribution of guanine nucleotide regulatory proteins to prostaglandin hyperalgesia in the rat

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

Cardiac sodium channels (hH1) are intrinsically more sensitive to block by lidocaine than are skeletal muscle (mu 1) channels

Common molecular determinants of local anesthetic, antiarrhythmic, and anticonvulsant block of voltage-gated Na+ channels

A tetrodotoxin-resistant voltage-gated sodium channel expressed by sensory neurons

Quantitative assessment of tactile allodynia in the rat paw

A new and sensitive method for measuring thermal nociception in cutaneous hyperalgesia

A novel behavioral model of neuropathic pain disorders produced in rats by partial sciatic nerve injury.

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

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William J. Martin

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7778390

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