2012
The NaV1.7 sodium channel: from molecule to man
Dib-Hajj SD, Yang Y, Black JA, Waxman SG. The NaV1.7 sodium channel: from molecule to man. Nature Reviews Neuroscience 2012, 14: 49-62. PMID: 23232607, DOI: 10.1038/nrn3404.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBiophysicsHumansModels, MolecularMutationNAV1.7 Voltage-Gated Sodium ChannelPainPeripheral NervesSignal TransductionSodium Channel BlockersTetrodotoxinConceptsDorsal hornPain disordersNerve endingsNociceptive dorsal root ganglion (DRG) neuronsPainful small fiber neuropathyDorsal root ganglion neuronsVoltage-gated sodium channel Nav1.7Small fiber neuropathyTreatment of painFree nerve endingsSecond-order neuronsSmall molecule blockersSodium channel Nav1.7Function mutationsOlfactory sensory neuronsProbability of neuronsNav1.7 sodium channelSuperficial laminaeGanglion neuronsRisk factorsSympathetic neuronsSlow depolarizationSpinal cordCardiac deficitsSensory neurons
2008
Mechanisms of Disease: sodium channels and neuroprotection in multiple sclerosis—current status
Waxman SG. Mechanisms of Disease: sodium channels and neuroprotection in multiple sclerosis—current status. Nature Reviews Neurology 2008, 4: 159-169. PMID: 18227822, DOI: 10.1038/ncpneuro0735.Peer-Reviewed Original Research
2004
Sodium channel blockers and axonal protection in neuroinflammatory disease
Waxman S. Sodium channel blockers and axonal protection in neuroinflammatory disease. Brain 2004, 128: 5-6. PMID: 15596795, DOI: 10.1093/brain/awh353.Peer-Reviewed Original Research
2003
The pentapeptide QYNAD does not block voltage-gated sodium channels
Cummins T, Renganathan M, Herzog R, Dib-Hajj S, Waxman S, Stys P, Horn R. The pentapeptide QYNAD does not block voltage-gated sodium channels. Neurology 2003, 60: 1871-1872. PMID: 12796562, DOI: 10.1212/wnl.60.11.1871-a.Peer-Reviewed Original Research
2002
HSV-1 Helper Virus 5dl1.2 Suppresses Sodium Currents in Amplicon-Transduced Neurons
White BH, Cummins TR, Wolf DH, Waxman SG, Russell DS, Kaczmarek LK. HSV-1 Helper Virus 5dl1.2 Suppresses Sodium Currents in Amplicon-Transduced Neurons. Journal Of Neurophysiology 2002, 87: 2149-2157. PMID: 11929932, DOI: 10.1152/jn.00498.2001.Peer-Reviewed Original ResearchConceptsSodium currentAnti-HSV antibodiesAverage spike frequencyWild-type HSV-1Helper virusViral-based strategiesDays of transductionCultured neuronsHSV-1Spike frequencyGene deliveryNeuronsMammalian neuronsAmplicon systemSimilar suppressionHSV-1 genesVirusTherapeutic purposesViral proteinsAmplicon preparationsCellsCoinfectionSuppressionPreparation resultsTiters
2000
Sodium channels and their genes: dynamic expression in the normal nervous system, dysregulation in disease states11Published on the World Wide Web on 15 August 2000.
Waxman S, Dib-Hajj S, Cummins T, Black J. Sodium channels and their genes: dynamic expression in the normal nervous system, dysregulation in disease states11Published on the World Wide Web on 15 August 2000. Brain Research 2000, 886: 5-14. PMID: 11119683, DOI: 10.1016/s0006-8993(00)02774-8.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsSodium channel gene expressionSodium channel geneChannel gene expressionChannel genesGene expressionPost-transcriptional levelNormal nervous systemSodium channel expressionSodium channelsChannel expressionMolecular plasticityGenesDynamic expressionCell membraneHypothalamic magnocellular neurosecretory neuronsDifferent repertoiresMultiple sclerosisNervous systemTherapeutic opportunitiesSodium channel subtypesExpressionElectrogenic propertiesRegulationChannel subtypesDysregulationA double mutation in families with periodic paralysis defines new aspects of sodium channel slow inactivation
Bendahhou S, Cummins T, Hahn A, Langlois S, Waxman S, Ptácek L. A double mutation in families with periodic paralysis defines new aspects of sodium channel slow inactivation. Journal Of Clinical Investigation 2000, 106: 431-438. PMID: 10930446, PMCID: PMC314328, DOI: 10.1172/jci9654.Peer-Reviewed Original ResearchConceptsChannel slow inactivationPeriodic paralysisSlow inactivationSodium channel slow inactivationMalignant hyperthermia susceptibilitySkeletal muscle disordersHuman skeletal muscleParalytic attacksMuscle disordersHyperkalemic periodic paralysisSkeletal muscleParalysisDisease-causing mutationsNovel mutationsHyperKPPChannel defectsMolecular determinantsAlpha subunitMutant channelsMutationsDouble mutationInactivationPatientsTransmembrane segments S5Do ‘demyelinating’ diseases involve more than myelin?
Waxman S. Do ‘demyelinating’ diseases involve more than myelin? Nature Medicine 2000, 6: 738-739. PMID: 10888913, DOI: 10.1038/77450.Peer-Reviewed Original Research
1996
Action potential-like responses in B 104 cells with low Na+ channel densities
Gu X, Waxman S. Action potential-like responses in B 104 cells with low Na+ channel densities. Brain Research 1996, 735: 50-58. PMID: 8905169, DOI: 10.1016/0006-8993(96)00604-x.Peer-Reviewed Original ResearchConceptsAction potential-like responsesB104 cellsWhole-cell patch-clamp methodB104 neuroblastoma cellsPA/pFCurrent-clamp modeSteady-state inactivationAction potential generationPatch-clamp methodMicroM TTXNeuroblastoma cellsPrepulse potentialPotential generationResponse amplitudeCellsResponseStimuli
1995
Sodium channel blockade by antibodies: A new mechanism of neurological disease?
Waxman S. Sodium channel blockade by antibodies: A new mechanism of neurological disease? Annals Of Neurology 1995, 37: 421-423. PMID: 7717678, DOI: 10.1002/ana.410370403.Peer-Reviewed Original Research