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  • Expression
  • Using Target Scan software, we discovered that SCN3A is the major target of miR-30b, and we then determined whether miR-30b regulated the expression of Nav1.3 by transfecting miR-30b agomir through the stimulation of TNF-α or by transfecting miR-30b antagomir in primary dorsal root ganglion (DRG) neurons. (frontiersin.org)
  • neurons
  • Our results showed that miR-30b agomir transfection down-regulated Nav1.3 mRNA stimulated with TNF-α in primary DRG neurons. (frontiersin.org)
  • NaV1.7
  • NaV1.7 flox'-Transgenic mouse expressing floxed NaV1.7 sodium channel gene (as described in Nassar et al. (uclb.com)
  • The four sodium channel subtypes that are of particular interest because of their restricted distribution in nociceptors are the tetrodotoxin-sensitive (TTX-S) channels NaV1.3 and NaV1.7 and the tetrodotoxin-resistant (TTX-R) channels NaV1.8 and NaV1.9. (uclb.com)
  • These channels are currently regarded as being amongst the best validated targets for pain therapy and in particular have caught widespread attention following the discovery of the remarkable analgesic phenotype associated with the loss-of-function NaV1.7 mutations in humans. (uclb.com)
  • The toxin-Nav1.7 complex is gradually dissociated upon prolonged strong depolarizations in a voltage-dependent manner, and the unbound toxin rebinds to Nav1.7 after a long repolarization. (uniprot.org)
  • Moreover, analysis of chimeric channels showed that the DIIS3-S4 linker is critical for toxin binding to Nav1.7. (uniprot.org)
  • These data are consistent with this toxin interacting with Nav1.7 site 4 and trapping the domain II voltage sensor in the closed state. (uniprot.org)
  • inhibition
  • Short extreme depolarizations partially activate the toxin-bound channel, indicating voltage-dependent inhibition of this toxin. (uniprot.org)
  • Consistent with this role, our electron microscopy results and immunocytochemical analysis show that Na v 1.4 and Na v 1.8 accumulate on phagosomes and that pharmacological inhibition of Na v channels as well as silencing the expression of Na v 1.4 with shRNA impairs the phagocytosis process. (springer.com)
  • genes
  • This genomic interval contains a cluster of sodium channel genes. (bmj.com)
  • Investigators from the University of British Columbia, Great Ormond Street Hospital for Children, and the National Hospital reported their findings on neurotransmitter deficiencies in two patients with mutations in voltage-gated sodium genes (SCN2A and SCN8A) discovered by whole exome sequencing. (readbyqxmd.com)
  • channelopathies
  • Sodium channels are associated with a large range of channelopathies among others epilepsy, Dravet syndrome, West syndrome, Irritable bowel syndrome, long QT syndrome, neuropsychiatric disorders, pain and insensitivity to pain. (sophion.com)
  • Genetic disorders that disrupt the function of these channels produce an array of Na(+) channelopathies resulting in neuronal impairment, chronic pain, neuromuscular pathologies, and cardiac arrhythmias. (readbyqxmd.com)
  • This chapter outlines sodium channel models with local anesthetics, anticonvulsants, and antiarrhythmics, which are used to manage pain and treat sodium channelopathies. (readbyqxmd.com)
  • local anesthetic
  • Because of their importance to the conduction of electrical signals, Na(+) channels are the target of a wide variety of local anesthetic, antiarrhythmic, anticonvulsant, and antidepressant drugs. (readbyqxmd.com)
  • roles
  • However, recent studies have shown the presence of Na v channels in several non-excitable cells, such as astrocytes and macrophages, demonstrating that the roles of these channels are more diverse than was previously thought. (springer.com)
  • differential
  • Several studies show an uneven distribution of ion channels and their differential regulation within dendrites and axons, which is a prerequisite for an appropriate integration of synaptic inputs and the generation of adequate action potential (AP) firing patterns. (frontiersin.org)