Neurotrophin-evoked depolarization requires the sodium channel Na(V)1.9
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A unique pathway for sustained neurotrophin signaling through an ankyrin-rich membrane-spanning proteinStepping Out of the Shade: Control of Neuronal Activity by the Scaffold Protein Kidins220/ARMSOverexpression of BDNF increases excitability of the lumbar spinal network and leads to robust early locomotor recovery in completely spinalized ratsA de novo gain-of-function mutation in SCN11A causes loss of pain perceptionEssential role of brain-derived neurotrophic factor in adult hippocampal function.Synaptic and extrasynaptic localization of brain-derived neurotrophic factor and the tyrosine kinase B receptor in cultured hippocampal neurons.Cochlear implants stimulate activity-dependent CREB pathway in the deaf auditory cortex: implications for molecular plasticity induced by neural prosthetic devicesNeurotrophic factors and neural prostheses: potential clinical applications based upon findings in the auditory system.Chronic depolarization enhances the trophic effects of brain-derived neurotrophic factor in rescuing auditory neurons following a sensorineural hearing loss.TRPC3 channels are necessary for brain-derived neurotrophic factor to activate a nonselective cationic current and to induce dendritic spine formation.BDNF induces calcium elevations associated with IBDNF, a nonselective cationic current mediated by TRPC channels.Mechanisms of nerve growth factor signaling in bone nociceptors and in an animal model of inflammatory bone pain.Neurobiology of local and intercellular BDNF signaling.The neurotrophin receptor p75NTR modulates long-term depression and regulates the expression of AMPA receptor subunits in the hippocampus.Activity-dependent release of endogenous BDNF from mossy fibers evokes a TRPC3 current and Ca2+ elevations in CA3 pyramidal neurons.Contribution of the tetrodotoxin-resistant voltage-gated sodium channel NaV1.9 to sensory transmission and nociceptive behavior.Polymorphisms of BDNF gene and autism spectrum disorders: family based association study with korean trios.A simple role for BDNF in learning and memory?Signaling receptome: a genomic and evolutionary perspective of plasma membrane receptors involved in signal transduction.Role of Na(v)1.9 in activity-dependent axon growth in motoneurons.Brain-derived neurotrophic factor induces NMDA receptor subunit one phosphorylation via ERK and PKC in the rat spinal cord.Protein synthesis and neurotrophin-dependent structural plasticity of single dendritic spines.p75 regulates Purkinje cell firing by modulating SK channel activity through Rac1.The roles of sodium channels in nociception: Implications for mechanisms of painFunctional properties and toxin pharmacology of a dorsal root ganglion sodium channel viewed through its voltage sensorsRegulation of neuronal survival and death by extracellular signals during development.Brain-derived neurotrophic factor and neuropsychiatric disorders.Epidermal growth factor, neurotrophins and the metastatic cascade in prostate cancer.Brain-derived neurotrophic factor mediates non-cell-autonomous regulation of sensory neuron position and identityNeurotrophin-mediated rapid signaling in the central nervous system: mechanisms and functions.Nerve growth factor in the hippocamposeptal system: evidence for activity-dependent anterograde delivery and modulation of synaptic activity.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.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 signalingRetrograde signaling in the optic nerve is necessary for electrical responsiveness of retinal ganglion cells.Transient receptor potential channels as novel effectors of brain-derived neurotrophic factor signaling: potential implications for Rett syndrome.Cell-autonomous axon growth of young motoneurons is triggered by a voltage-gated sodium channelBrain-derived neurotrophic factor-dependent unmasking of "silent" synapses in the developing mouse barrel cortex.A new mouse model of inducible, chronic retinal ganglion cell dysfunction not associated with cell death.
P2860
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P2860
Neurotrophin-evoked depolarization requires the sodium channel Na(V)1.9
description
2002 nî lūn-bûn
@nan
2002 թուականի Հոկտեմբերին հրատարակուած գիտական յօդուած
@hyw
2002 թվականի հոտեմբերին հրատարակված գիտական հոդված
@hy
2002年の論文
@ja
2002年論文
@yue
2002年論文
@zh-hant
2002年論文
@zh-hk
2002年論文
@zh-mo
2002年論文
@zh-tw
2002年论文
@wuu
name
Neurotrophin-evoked depolarization requires the sodium channel Na(V)1.9
@ast
Neurotrophin-evoked depolarization requires the sodium channel Na(V)1.9
@en
Neurotrophin-evoked depolarization requires the sodium channel Na(V)1.9
@nl
type
label
Neurotrophin-evoked depolarization requires the sodium channel Na(V)1.9
@ast
Neurotrophin-evoked depolarization requires the sodium channel Na(V)1.9
@en
Neurotrophin-evoked depolarization requires the sodium channel Na(V)1.9
@nl
prefLabel
Neurotrophin-evoked depolarization requires the sodium channel Na(V)1.9
@ast
Neurotrophin-evoked depolarization requires the sodium channel Na(V)1.9
@en
Neurotrophin-evoked depolarization requires the sodium channel Na(V)1.9
@nl
P2860
P3181
P356
P1433
P1476
Neurotrophin-evoked depolarization requires the sodium channel Na(V)1.9
@en
P2093
Karl W Kafitz
Robert Blum
P2860
P2888
P304
P3181
P356
10.1038/NATURE01085
P407
P577
2002-10-17T00:00:00Z
P5875
P6179
1017263066