Nerve injury induces robust allodynia and ectopic discharges in Nav1.3 null mutant mice. - Wikidata - awgldk - TriplyDB

Nerve injury induces robust allodynia and ectopic discharges in Nav1.3 null mutant mice.

Nerve injury induces robust allodynia and ectopic discharges in Nav1.3 null mutant mice.

http://www.wikidata.org/entity/Q35121209

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Pain as a channelopathy Conotoxins That Could Provide Analgesia through Voltage Gated Sodium Channel Inhibition Global Nav1.7 knockout mice recapitulate the phenotype of human congenital indifference to pain Inhibition of Inactive States of Tetrodotoxin-Sensitive Sodium Channels Reduces Spontaneous Firing of C-Fiber Nociceptors and Produces Analgesia in Formalin and Complete Freund's Adjuvant Models of Pain Voltage-gated Na+ channels in neuropathic pain.Voltage-gated sodium channel expression in mouse DRG after SNI leads to re-evaluation of projections of injured fibers.[EXPRESS] Ion channels and neuronal hyperexcitability in chemotherapy-induced peripheral neuropathy; cause and effect?Intrathecal lidocaine pretreatment attenuates immediate neuropathic pain by modulating Nav1.3 expression and decreasing spinal microglial activation Significant determinants of mouse pain behaviour.Tetrodotoxin (TTX) as a therapeutic agent for pain.The blockade of the transient receptor potential vanilloid type 1 and fatty acid amide hydrolase decreases symptoms and central sequelae in the medial prefrontal cortex of neuropathic rats Ion channel pharmacology.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 Local knockdown of the NaV1.6 sodium channel reduces pain behaviors, sensory neuron excitability, and sympathetic sprouting in rat models of neuropathic pain.Novel sodium channel antagonists in the treatment of neuropathic pain.The role of sodium channels in chronic pain.Virus-Mediated Knockdown of Nav1.3 in Dorsal Root Ganglia of STZ-Induced Diabetic Rats Alleviates Tactile Allodynia.Conotoxins targeting neuronal voltage-gated sodium channel subtypes: potential analgesics?Virus-mediated shRNA knockdown of Na(v)1.3 in rat dorsal root ganglion attenuates nerve injury-induced neuropathic pain Blocking sodium channels to treat neuropathic pain.Voltage-gated sodium channel blockers for the treatment of neuropathic pain.Na(+) channel blockers for the treatment of pain: context is everything, almost.Presynaptic and postsynaptic amplifications of neuropathic pain in the anterior cingulate cortex.Neuropathic pain: a maladaptive response of the nervous system to damage.Sodium channel blockers for the treatment of neuropathic pain.Subtype-selective targeting of voltage-gated sodium channels.Pain channelopathies.Sodium channel gene family: epilepsy mutations, gene interactions and modifier effects.Isoform-selective voltage-gated Na(+) channel modulators as next-generation analgesics.Ion channel blockers for the treatment of neuropathic pain.Recent developments regarding voltage-gated sodium channel blockers for the treatment of inherited and acquired neuropathic pain syndromes.Deconstructing the neuropathic pain phenotype to reveal neural mechanisms.Genetic aspects of sodium channelopathy in small fiber neuropathy.Advances in targeting voltage-gated sodium channels with small molecules.Neurological perspectives on voltage-gated sodium channels.New and developing drugs for the treatment of neuropathic pain in diabetes.Genotype phenotype associations across the voltage-gated sodium channel family.Pain without nociceptors? Nav1.7-independent pain mechanisms.Identification of sodium channel isoforms that mediate action potential firing in lamina I/II spinal cord neurons.

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P2860

Nerve injury induces robust allodynia and ectopic discharges in Nav1.3 null mutant mice.

http://www.wikidata.org/entity/Q35121209

description

2006 nî lūn-bûn

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2006 թուականի Հոկտեմբերին հրատարակուած գիտական յօդուած

@hyw

2006 թվականի հոտեմբերին հրատարակված գիտական հոդված

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2006年の論文

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2006年学术文章

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2006年学术文章

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2006年学术文章

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2006年学术文章

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2006年学术文章

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2006年學術文章

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name

Nerve injury induces robust allodynia and ectopic discharges in Nav1.3 null mutant mice.

@ast

Nerve injury induces robust allodynia and ectopic discharges in Nav1.3 null mutant mice.

@en

type

label

Nerve injury induces robust allodynia and ectopic discharges in Nav1.3 null mutant mice.

@ast

Nerve injury induces robust allodynia and ectopic discharges in Nav1.3 null mutant mice.

@en

prefLabel

Nerve injury induces robust allodynia and ectopic discharges in Nav1.3 null mutant mice.

@ast

Nerve injury induces robust allodynia and ectopic discharges in Nav1.3 null mutant mice.

@en

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Nerve injury induces robust allodynia and ectopic discharges in Nav1.3 null mutant mice

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Alessandra Levato

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Giovanna Mallucci

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John N Wood

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Mark D Baker

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Mohammed A Nassar

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Rachel Ingram

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P2860

Nociceptor-specific gene deletion reveals a major role for Nav1.7 (PN1) in acute and inflammatory pain

Replicate high-density rat genome oligonucleotide microarrays reveal hundreds of regulated genes in the dorsal root ganglion after peripheral nerve injury

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

Upregulation of sodium channel Nav1.3 and functional involvement in neuronal hyperexcitability associated with central neuropathic pain after spinal cord injury

A cre-transgenic mouse strain for the ubiquitous deletion of loxP-flanked gene segments including deletion in germ cells

The changes in expression of three subtypes of TTX sensitive sodium channels in sensory neurons after spinal nerve ligation.

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

Sodium channels and their genes: dynamic expression in the normal nervous system, dysregulation in disease states(1).

Acquired channelopathies in nerve injury and MS.

Na+ channel immunolocalization in peripheral mammalian axons and changes following nerve injury and neuroma formation.

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10.1186/1744-8069-2-33

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Stephen B McMahon

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