IndraLab

Statements


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"We show that in male rat dorsal root ganglion (DRG) neurons these mutations, which impair inactivation, significantly increase TTX-resistant resurgent sodium currents mediated by Nav1.8."

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"In a rat model of neuropathic pain, expression of Nav1.8 in axons is sufficiently up-regulated to allow TTX-resistant propagation of action potentials in some C-fibers , but it remains unclear under what conditions Nav1.8 inhibition can inhibit generation or propagation of action potentials in human pain conditions."

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"The novel sodium channel PN3/alpha-SNS, which was cloned from a rat dorsal root ganglion (DRG) cDNA library, is expressed predominantly in small sensory neurons and may contribute to the tetrodotoxin-resistant (TTXR) sodium current that is believed to be associated with central sensitization in chronic neuropathic pain states."

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"Both Nav1.3 and Nav1.8 had previously been shown to increase the current densities of tetrodotoxin-sensitive and tetrodotoxin-resistant Na channels in DRG neurons by TNF-α."

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"It has been shown that activation of p38 MAPK increases TTX-resistant sodium channel currents by phosphorylation of L1 loop serines of Nav1.8 channels [47]."

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"TTX resistance is predominantly mediated by SCN10A (also known as Na 1.8)."