2023
Conserved but not critical: Trafficking and function of NaV1.7 are independent of highly conserved polybasic motifs
Tyagi S, Sarveswaran N, Higerd-Rusli G, Liu S, Dib-Hajj F, Waxman S, Dib-Hajj S. Conserved but not critical: Trafficking and function of NaV1.7 are independent of highly conserved polybasic motifs. Frontiers In Molecular Neuroscience 2023, 16: 1161028. PMID: 37008789, PMCID: PMC10060856, DOI: 10.3389/fnmol.2023.1161028.Peer-Reviewed Original ResearchSensory axonsPeripheral voltage-gated sodium channelsMajor unmet clinical needFunction of Nav1.7Non-addictive treatmentsUnmet clinical needVoltage-clamp recordingsVoltage-gated sodium channelsPain therapyChronic painPrimary afferentsNoxious stimuliTherapeutic modalitiesAction potentialsAxonal transportClinical needVesicular packagingSodium channelsHuman painPainAxonal traffickingAxonal surfaceAxonal membraneAxonsAttractive targetPaclitaxel effects on axonal localization and vesicular trafficking of NaV1.8
Baker C, Tyagi S, Higerd-Rusli G, Liu S, Zhao P, Dib-Hajj F, Waxman S, Dib-Hajj S. Paclitaxel effects on axonal localization and vesicular trafficking of NaV1.8. Frontiers In Molecular Neuroscience 2023, 16: 1130123. PMID: 36860665, PMCID: PMC9970094, DOI: 10.3389/fnmol.2023.1130123.Peer-Reviewed Original ResearchChemotherapy-induced peripheral neuropathyDorsal root gangliaPTX treatmentDRG axonsEffect of paclitaxelVoltage-gated sodium channel NaPain syndromePeripheral neuropathyDRG neuronsSodium channel NaRoot gangliaCell cycle arrestNeuronal somataSensory neuronsSide effectsTherapeutic targetingTumor growthPaclitaxel effectAntineoplastic agentsAxonal localizationPaclitaxelNumber of NaAxonal compartmentAxonsChannel Na
2014
Epidermal Nerve Fibers
Lauria G, Merkies I, Waxman S, Faber C. Epidermal Nerve Fibers. 2014, 76-79. DOI: 10.1016/b978-0-12-385157-4.00656-4.Peer-Reviewed Original ResearchEpidermal nerve fibersNerve fibersNeuropathic painSkin biopsiesProtein gene product 9.5Severity of neuropathySmall fiber neuropathySmall nerve fibersDistinct clinical syndromeSensory nervesClinical syndromeProduct 9.5Unmyelinated axonsNeuropathyPainAvailability of antibodiesBiopsySomatic functionsInnervationNociceptorsNerveSyndromeAxonsDegenerationDiagnosis
2012
Gain-of-function Nav1.8 mutations in painful neuropathy
Faber CG, Lauria G, Merkies IS, Cheng X, Han C, Ahn HS, Persson AK, Hoeijmakers JG, Gerrits MM, Pierro T, Lombardi R, Kapetis D, Dib-Hajj SD, Waxman SG. Gain-of-function Nav1.8 mutations in painful neuropathy. Proceedings Of The National Academy Of Sciences Of The United States Of America 2012, 109: 19444-19449. PMID: 23115331, PMCID: PMC3511073, DOI: 10.1073/pnas.1216080109.Peer-Reviewed Original ResearchConceptsPainful peripheral neuropathySmall fiber neuropathyPainful neuropathyPeripheral neuropathyPainful small fiber neuropathyDorsal root ganglion neuronsSodium channelsApparent underlying causePeripheral nerve axonsDRG neuronsGanglion neuronsNeuropathyNerve axonsUnderlying causeFunction variantsCurrent clampPatientsPotential pathogenicityNeuronsMutationsHyperexcitabilityAxonsResponse
2006
Dysfunction and recovery in demyelinated and dysmyelinated axons
Waxman S. Dysfunction and recovery in demyelinated and dysmyelinated axons. 2006, 468-486. DOI: 10.1017/cbo9780511545061.029.Peer-Reviewed Original Research
2005
7 Altered Distributions and Functions of Multiple Sodium Channel Subtypes in Multiple Sclerosis and its Models
Waxman S. 7 Altered Distributions and Functions of Multiple Sodium Channel Subtypes in Multiple Sclerosis and its Models. 2005, 101-118. DOI: 10.1016/b978-012738761-1/50008-0.Peer-Reviewed Original ResearchMultiple sclerosisSodium channel subtypesVoltage-gated sodium channelsSodium channelsChannel subtypesDistinct voltage-gated sodium channelsPathophysiology of MSAxonal degenerationTherapeutic strategiesSclerosisFiring patternsExperimental modelMaladaptive roleNeuronal signalingSubtypesMolecular analysisAltered distributionNeuronsRecent studiesMajor contributorPathophysiologyAxonsDegenerationDiseaseImportant role6 The Conduction Properties of Demyelinated and Remyelinated Axons
Smith K, Waxman S. 6 The Conduction Properties of Demyelinated and Remyelinated Axons. 2005, 85-100. DOI: 10.1016/b978-012738761-1/50007-9.Peer-Reviewed Original ResearchRestoration of conductionConduction blockDemyelination-induced conduction blockExperimental demyelinating lesionsDemyelinating lesionsSegmental demyelinationMyelin thinningDemyelinated axonsElectrophysiological featuresConduction failureAxonal functionElectrophysiological propertiesDemyelinationAxonsMyelinLesionsIon channel populationsDemyelinated membraneChannel populationsAdaptive responseComplete loss
2004
Chapter 5 Electrophysiologic Consequences of Myelination
Waxman S, Bangalore L. Chapter 5 Electrophysiologic Consequences of Myelination. 2004, 117-141. DOI: 10.1016/b978-012439510-7/50058-9.Peer-Reviewed Original ResearchImpulse conductionConduction abnormalitiesDemyelinated axonsRole of demyelinationRestoration of conductionTotal conduction blockNew therapeutic interventionsHigh-frequency trainsEntire myelin sheathMyelin lossClinical deficitsElectrophysiologic consequencesConduction blockPharmacological modulationConduction velocityTherapeutic interventionsAction potentialsDemyelinationMyelin sheathAxonsMolecular substratesSymptom productionAxonal membraneAbnormalitiesCurrent strategies
2002
Sodium channels and the molecular basis for pain
Black J, Cummins T, Dib-Hajj S, Waxman S. Sodium channels and the molecular basis for pain. Progress In Inflammation Research 2002, 23-50. DOI: 10.1007/978-3-0348-8129-6_2.ChaptersPrimary sensory neuronsSensory neuronsAction potentialsSpontaneous action potentialsHigh-frequency activityInflammatory painTrigeminal neuronsNociceptive responsesAscending pathwaysPeripheral nervesTissue injuryNoxious stimuliPeripheral targetsPainNeuronsSodium channelsTemperature sensationBrainHigh thresholdNerveMolecular basisInjuryAxonsDRG
2001
Direct Interaction with Contactin Targets Voltage-gated Sodium Channel Nav1.9/NaN to the Cell Membrane*
Liu C, Dib-Hajj S, Black J, Greenwood J, Lian Z, Waxman S. Direct Interaction with Contactin Targets Voltage-gated Sodium Channel Nav1.9/NaN to the Cell Membrane*. Journal Of Biological Chemistry 2001, 276: 46553-46561. PMID: 11581273, DOI: 10.1074/jbc.m108699200.Peer-Reviewed Original ResearchConceptsDorsal root gangliaRoot gangliaSodium channelsSmall sensory neuronsVoltage-gated sodium channelsTrigeminal ganglionNerve endingsC-fibersSensory neuronsNeuron somataChinese hamster ovary cell lineDifferent physiological propertiesGangliaHamster ovary cell lineNeuronal membranesChinese hamster ovary cellsOvary cell lineProtein complexesSurface expressionHamster ovary cellsCell linesAxonsSurface localizationCell membraneOvary cells
2000
Experimental Approaches to Restoration of Function of Ascending and Descending Axons in Spinal Cord Injury
Waxman S, Kocsis J. Experimental Approaches to Restoration of Function of Ascending and Descending Axons in Spinal Cord Injury. Contemporary Neuroscience 2000, 215-239. DOI: 10.1007/978-1-59259-200-5_10.Peer-Reviewed Original ResearchSpinal cord injuryRestoration of functionCord injuryDemyelinated spinal cord axonsSpinal cord traumaResult of demyelinationSpinal cord axonsSubpopulation of axonsNormal action potentialCord traumaResidual axonsAxonal conductionSpinal cordConduction blockDescending axonsSCI researchAction potentialsAxonsDemyelinationInjurySignificant factorLocalization of the tetrodotoxin-resistant sodium channel NaN in nociceptors
Fjell J, Hjelmström P, Hormuzdiar W, Milenkovic M, Aglieco F, Tyrrell L, Dib-Hajj S, Waxman S, Black J. Localization of the tetrodotoxin-resistant sodium channel NaN in nociceptors. Neuroreport 2000, 11: 199-202. PMID: 10683857, DOI: 10.1097/00001756-200001170-00039.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceAnimalsAxonsCorneaFemaleGanglia, SpinalImage Processing, Computer-AssistedImmunohistochemistryMolecular Sequence DataMyelin SheathNAV1.9 Voltage-Gated Sodium ChannelNerve FibersNeurons, AfferentNeuropeptidesNociceptorsPresynaptic TerminalsRanvier's NodesRatsRats, Sprague-DawleySciatic NerveSodium ChannelsTetrodotoxinConceptsSciatic nerveSmall diameter primary sensory neuronsSodium currentTetrodotoxin-resistant sodium channelsTetrodotoxin-resistant sodium currentDorsal root ganglion neuronsSodium channelsPrimary sensory neuronsAxonal sodium currentsNodes of RanvierNociceptive transmissionChannel immunoreactivityGanglion neuronsUnmyelinated fibersAxon terminalsSensory neuronsNerveImmunoreactivityAxonsNeuronsSpecific peptidesNociceptorsIB4CorneaAntibodies
1998
Transplanted Olfactory Ensheathing Cells Remyelinate and Enhance Axonal Conduction in the Demyelinated Dorsal Columns of the Rat Spinal Cord
Imaizumi T, Lankford K, Waxman S, Greer C, Kocsis J. Transplanted Olfactory Ensheathing Cells Remyelinate and Enhance Axonal Conduction in the Demyelinated Dorsal Columns of the Rat Spinal Cord. Journal Of Neuroscience 1998, 18: 6176-6185. PMID: 9698311, PMCID: PMC2605360, DOI: 10.1523/jneurosci.18-16-06176.1998.Peer-Reviewed Original ResearchConceptsDorsal column axonsRat spinal cordSpinal cordRemyelinated axonsDorsal columnsAdult rat spinal cordExtent of remyelinationTransplantation of OECsSpinal cord lesionsCell injection siteQuantitative histological analysisFunctional remyelinationCord lesionsAxonal conductionNeonatal ratsFocal injectionsConduction blockSchwann cellsConduction velocityInjection siteElectrophysiological propertiesAction potentialsAxonsHistological analysisTransplantation
1997
Immunolocalization of the Na+–Ca2+ exchanger in mammalian myelinated axons
Steffensen I, Waxman S, Mills L, Stys P. Immunolocalization of the Na+–Ca2+ exchanger in mammalian myelinated axons. Brain Research 1997, 776: 1-9. PMID: 9439790, DOI: 10.1016/s0006-8993(97)00868-8.Peer-Reviewed Original ResearchConceptsOptic nerveSpinal cordDorsal root axonsSciatic nerve sectionRat optic nerveCentral myelinated axonsCardiac type IFiner processesSimilar staining patternNerve sectionDorsal columnsSciatic nerveFrozen cryostat sectionsAnoxic injuryAxonal profilesImmunofluorescence labeling techniqueMyelinated axonsCell bodiesCryostat sectionsImportant mediatorAxonal localizationMammalian axonsNerveAxonsStaining patternFunctional Repair of Myelinated Fibers in the Spinal Cord by Transplantation of Glial Cells
Waxman S, Kocsis J. Functional Repair of Myelinated Fibers in the Spinal Cord by Transplantation of Glial Cells. Altschul Symposia Series 1997, 283-298. DOI: 10.1007/978-1-4615-5949-8_28.Peer-Reviewed Original ResearchConduction velocityMyelinated axonsMyelin sheathNon-myelinated fibresClinical deficitsMyelin damageConduction abnormalitiesDemyelinated axonsSpinal cordGlial cellsMyelinated fibersConduction blockSynaptic terminalsAction potentialsRefractory periodCell bodiesDemyelinated fibersAxonsFunctional repair
1995
Anoxic/ischemic injury in axons
STYS P, RANSOM B, BLACK J, WAXMAN S. Anoxic/ischemic injury in axons. 1995, 462-479. DOI: 10.1093/acprof:oso/9780195082937.003.0024.Peer-Reviewed Original ResearchNerve fibersNervous systemAnoxic/ischemic injuryPeripheral nervous systemAnoxia/ischemiaCentral nervous systemIschemic injuryPeripheral axonsAction potential propagationAxonsNormal functionPathological statesBiochemical homeostasisTransmembrane ion gradientsCellular energy metabolismInjuryEnergy metabolismPotential propagationSurvivalHuman diseasesMajor mechanismIon gradientsMembrane polarizationIschemiaDiseaseVoltage-gated ion channels in axons: Localization, function, and development
WAXMAN S. Voltage-gated ion channels in axons: Localization, function, and development. 1995, 218-243. DOI: 10.1093/acprof:oso/9780195082937.003.0011.Peer-Reviewed Original Research
1994
Anoxic injury of rat optic nerve: ultrastructural evidence for coupling between Na+ influx and Ca2+-mediated injury in myelinated CNS axons
Waxman S, Black J, Ransom B, Stys P. Anoxic injury of rat optic nerve: ultrastructural evidence for coupling between Na+ influx and Ca2+-mediated injury in myelinated CNS axons. Brain Research 1994, 644: 197-204. PMID: 8050031, DOI: 10.1016/0006-8993(94)91680-2.Peer-Reviewed Original ResearchConceptsOptic nerveOptic nerve axonsRat optic nerveNerve axonsBrain slice chamberCompound action potentialLoss of cristaeMicroM tetrodotoxinAnoxic injuryNormoxic controlsNerveAstrocyte processesPerinodal astrocyte processesWhite matterMyelinated axonsAstrocytic processesCNS axonsTetrodotoxinAction potentialsSlice chamberAxonsLoss of microtubulesCytoskeletal damageInjuryNormoxic conditionsAnoxic Injury of Central Myelinated Axons: Nonsynaptic Ionic Mechanisms
Ransom B, Waxman S, Stys P. Anoxic Injury of Central Myelinated Axons: Nonsynaptic Ionic Mechanisms. 1994, 77-90. DOI: 10.1007/978-3-642-78151-3_9.Peer-Reviewed Original ResearchGlial cellsAnoxic injuryWhite matterCentral nervous system traumaIrreversible anoxic injuryPathophysiology of strokeNervous system traumaCentral myelinated axonsNeuronal cell bodiesAnoxia/ischemiaGray matter areasCNS axonal injuryNeuronal injuryIonic mechanismsAxonal injurySystem traumaCell injuryMyelinated axonsInjuryCell bodiesAxonsMatter areasBrainMetabolic substratesReliable model system