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
2006
A single sodium channel mutation produces hyper- or hypoexcitability in different types of neurons
Rush AM, Dib-Hajj SD, Liu S, Cummins TR, Black JA, Waxman SG. A single sodium channel mutation produces hyper- or hypoexcitability in different types of neurons. Proceedings Of The National Academy Of Sciences Of The United States Of America 2006, 103: 8245-8250. PMID: 16702558, PMCID: PMC1472458, DOI: 10.1073/pnas.0602813103.Peer-Reviewed Original ResearchConceptsNeuronal cell typesCell typesChannel mutationsSympathetic neuronsMembrane potentialDifferent cell typesSodium channel mutationsMolecular basisNeuropathic pain syndromesIon channel mutationsSympathetic ganglion neuronsTypes of neuronsSingle mutationSodium channel Nav1.7Ion channelsMutationsPain syndromeSympathetic dysfunctionGanglion neuronsNav1.8 channelsSensory neuronsFunctional effectsChannel Nav1.7HypoexcitabilityNeurons