2018
Atypical changes in DRG neuron excitability and complex pain phenotype associated with a Nav1.7 mutation that massively hyperpolarizes activation
Huang J, Mis MA, Tanaka B, Adi T, Estacion M, Liu S, Walker S, Dib-Hajj SD, Waxman SG. Atypical changes in DRG neuron excitability and complex pain phenotype associated with a Nav1.7 mutation that massively hyperpolarizes activation. Scientific Reports 2018, 8: 1811. PMID: 29379075, PMCID: PMC5788866, DOI: 10.1038/s41598-018-20221-7.Peer-Reviewed Original ResearchConceptsNav1.7 mutationClinical presentationDRG neuronsPain sensationDorsal root ganglion neuronsDRG neuron excitabilityFunction Nav1.7 mutationsLoss of excitabilityAbsence of painSodium channel Nav1.7Function mutationsComplex pain phenotypesEpisodic painSevere painCorneal anesthesiaGanglion neuronsNeuron excitabilityClinical lossPain phenotypesPainChannel Nav1.7Atypical changesNav1.7 channelsClinical levelNeurons
2004
Contactin Associates with Sodium Channel Nav1.3 in Native Tissues and Increases Channel Density at the Cell Surface
Shah BS, Rush AM, Liu S, Tyrrell L, Black JA, Dib-Hajj SD, Waxman SG. Contactin Associates with Sodium Channel Nav1.3 in Native Tissues and Increases Channel Density at the Cell Surface. Journal Of Neuroscience 2004, 24: 7387-7399. PMID: 15317864, PMCID: PMC6729770, DOI: 10.1523/jneurosci.0322-04.2004.Peer-Reviewed Original ResearchConceptsAxotomized DRG neuronsDRG neuronsAxotomized dorsal root ganglion (DRG) neuronsDorsal root ganglion neuronsSodium channel Nav1.3Sodium channelsVoltage-gated sodium channelsHuman embryonic kidney 293 cellsNeuropathic painEmbryonic kidney 293 cellsGanglion neuronsSciatic nerveCell surfaceCell adhesion moleculeRat brainContactin/F3Kidney 293 cellsHEK-293 cellsAdhesion moleculesNeuronsElevated levelsSurface expressionContactinUpregulationCotransfected cells