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We find that approximately 80% of neurons responsive to cold down to 1 degrees C do not express NaV1.8, and that the genetic deletion of NaV1.8 does not affect the relative number, distribution, or maximal response of cold-sensitive neurons. Furthermore, the deletion of NaV1.8 had no observable effect on transient cold-induced (>/=5 degrees C) behaviors in mice, as measured by the cold-plantar, cold-plate (5 and 10 deg...
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Nav1.8 role in the inflammatory pain.CXCL13, upregulated by peripheral inflammation, acts on CXCR5 on dorsal root ganglia neurons and activates p38, which increases Nav1.8 current density and further contributes to the maintenance of inflammatory pain.
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Data suggests that increases in the expression of Nav1.8 channels, regulatory beta1 subunits and TNF receptor 1 contribute to increased nociceptor excitability and hyperalgesia in the tumor necrosis factor transgenic mice.
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that ectopic NaV1.8 expression precipitates depolarizing conduction failure in Charcot-Marie-Tooth disease
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While Scn10a transcripts are not detectible in ventricular cardiomyocytes, gene deletion results in reproducible loss of late sodium current under extreme experimental conditions. However, there are no identifiable consequences of this Scn10a deletion in the intact mouse heart at usual rates.
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Results suggest that Nav1.8 plays a role in modulating specific aspects of the retinal physiology and that starburst amacrine cells are a fundamental cellular contributor to the oscillatory potentials in mice, a clear demonstration of the dichotomy between electroretinogram b-wave and oscillatory potentials.
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These preclinical proof-of-concept data suggest that PF-01247324, its derivatives, or other Nav1.8-selective blockers merit further study for providing symptomatic therapy for cerebellar dysfunction in MS and related disorders.
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A novel splice variant of SCN10A lacking exon 11 was found in human but not detected in mouse or rat.
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Nav1.8 gain-of-function point mutation contributes to intense hyperexcitability along the afferent axon within distinct sensory neuron subtypes.
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Nav1.8 interacts with ankyrin G and they co-localize in skin nerve fibers.
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The enhanced NaV1.8 activity are essential for the development of long-lasting hyperalgesia in acid-induced, chronic, widespread muscle pain.
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Analysis of BAC transgenic strains harboring an engineered deletion of the enhancer within Scn10a revealed that the enhancer was essential for Scn5a expression in cardiac tissue. SCN10A variant rs6801957 modulated Scn5a expression in the heart.
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regulation of Nav 1.8 expression and the excitability of nociceptive primary afferent neurons may be involved in the underlying mechanisms
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Nav1.8 expression increases in dorsal root ganglion neurons following pretreatment with CC chemokine ligand 2.
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We demonstrate that 75% of dorsal root ganglion (DRG) neurons express Na(v)1.8-Cre, including >90% of neurons expressing markers of nociceptors.
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Behavioural deficits in Nav1.7/Nav1.8 knockout mice reflects a failure of action potential propagation in a mechanosensitive set of sensory neurons rather than a loss of primary transduction currents.
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The functional presence of SCN10A/Nav1.8 in intracardiac neurons is demonstrated, indicating a novel role for this neuronal sodium channel in regulation of cardiac electric activity.
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identification of enhancers in the Scn5a/Scn10a locus, regulated by TBX3 and TBX5
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These results demonstrate increased expression levels of Nav1.7, Nav1.8, and perhaps Nav1.1 in the dorsal root ganglia in mice with a heterozygous mutation of the Nf1 gene
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PKCepsilon phosphorylated NaV1.8 at S1452. Alanine substitution at this site blocked PKCepsilon modulation of channel properties. NaV1.8 is an important, direct substrate of PKCepsilon that mediates PKCepsilon-dependent mechanical hyperalgesia.
