2018
Therapeutic potential of Pak1 inhibition for pain associated with cutaneous burn injury
Guo Y, Benson C, Hill M, Henry S, Effraim P, Waxman S, Dib-Hajj S, Tan AM. Therapeutic potential of Pak1 inhibition for pain associated with cutaneous burn injury. Molecular Pain 2018, 14: 1744806918788648. PMID: 29956587, PMCID: PMC6053256, DOI: 10.1177/1744806918788648.Peer-Reviewed Original ResearchConceptsDendritic spine dysgenesisNeuropathic painSpine dysgenesisBurn injurySignificant tactile allodyniaDorsal horn neuronsChronic disease burdenActivity-dependent expressionCutaneous burn injurySecond-degree burn injuryBurn injury modelC-fos expressionPotential molecular targetsDrug discontinuationHeat hyperalgesiaTactile allodyniaDorsal hornPain outcomesChronic painNociceptive activityLower painDisease burdenInjury modelCognitive dysfunctionPain
2009
The ataxia3 Mutation in the N-Terminal Cytoplasmic Domain of Sodium Channel Nav1.6 Disrupts Intracellular Trafficking
Sharkey LM, Cheng X, Drews V, Buchner DA, Jones JM, Justice MJ, Waxman SG, Dib-Hajj SD, Meisler MH. The ataxia3 Mutation in the N-Terminal Cytoplasmic Domain of Sodium Channel Nav1.6 Disrupts Intracellular Trafficking. Journal Of Neuroscience 2009, 29: 2733-2741. PMID: 19261867, PMCID: PMC2679640, DOI: 10.1523/jneurosci.6026-08.2009.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBlotting, WesternCell LineChromosome MappingCytoplasmData Interpretation, StatisticalDNA, ComplementaryElectrophysiologyEthylnitrosoureaImmunohistochemistryMachado-Joseph DiseaseMiceMice, Inbred C57BLMutagensMutationMutation, MissenseNAV1.6 Voltage-Gated Sodium ChannelNerve Tissue ProteinsPatch-Clamp TechniquesSciatic NerveSodium ChannelsSubcellular FractionsTransfectionConceptsMutant channelsCytoplasmic N-terminal regionN-terminal cytoplasmic domainCytoplasmic N-terminal domainMouse chromosome 15N-terminal domainN-terminal regionAmino acid substitution p.Primary cerebellar granule cellsVoltage-dependent inward sodium currentMutant proteinsCytoplasmic domainJuvenile lethalityCis-GolgiTrafficking defectsPlasma membraneSodium channelsIntracellular traffickingProtein abundanceWild typeN-terminusGolgi complexMutant transcriptsChromosome 15Whole-cell patch-clamp studies
2006
Axonal conduction and injury in multiple sclerosis: the role of sodium channels
Waxman SG. Axonal conduction and injury in multiple sclerosis: the role of sodium channels. Nature Reviews Neuroscience 2006, 7: 932-941. PMID: 17115075, DOI: 10.1038/nrn2023.Peer-Reviewed Original ResearchConceptsAxonal degenerationSodium channelsChannel isoformsDistinct pathophysiological rolesKey PointsMultiple sclerosisMultiple neurological deficitsRelapsing-remitting courseRestoration of conductionDegeneration of axonsCerebellar Purkinje neuronsVoltage-gated sodium channelsContext of demyelinationNeurological deficitsProgressive courseMultiple sclerosisAxonal conductionDisease progressionNav1.8 channelsConduction failurePathophysiological rolePurkinje neuronsCNS axonsFiring patternsLoss of coordinationAberrant expressionFire and phantoms after spinal cord injury: Na+ channels and central pain
Waxman S, Hains B. Fire and phantoms after spinal cord injury: Na+ channels and central pain. Trends In Neurosciences 2006, 29: 207-215. PMID: 16494954, DOI: 10.1016/j.tins.2006.02.003.Peer-Reviewed Original ResearchConceptsSpinal cord injuryNeuropathic painCord injurySpinal cord dorsal horn neuronsDorsal horn neuronsNervous system injuryCentral painPain pathwaysSystem injuryThalamic neuronsPainAbnormal expressionPhantom phenomenaNeuronsInjuryMolecular targetsMolecular changesRecent findingsHyperexcitabilityNav1.3Molecular basis
2001
β1 adducin gene expression in DRG is developmentally regulated and is upregulated by glial-derived neurotrophic factor and nerve growth factor
Ghassemi F, Dib-Hajj S, Waxman S. β1 adducin gene expression in DRG is developmentally regulated and is upregulated by glial-derived neurotrophic factor and nerve growth factor. Brain Research 2001, 90: 118-124. PMID: 11406290, DOI: 10.1016/s0169-328x(01)00091-2.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCalmodulin-Binding ProteinsCells, CulturedCytoskeletonGanglia, SpinalGene Expression ProfilingGene Expression Regulation, DevelopmentalGlial Cell Line-Derived Neurotrophic FactorNerve Growth FactorNerve Growth FactorsNerve Tissue ProteinsNeurons, AfferentNeuroprotective AgentsRatsRats, Sprague-DawleyReverse Transcriptase Polymerase Chain ReactionConceptsGlial-derived neurotrophic factorReal-time reverse transcription-polymerase chain reactionNeurotrophic factorTrigeminal ganglionDRG culturesRat DRGGrowth factorDorsal root ganglion culturesAdult rat DRGRat dorsal root ganglion culturesSuperior cervical ganglionReverse transcription-polymerase chain reactionExpression levelsNerve growth factorNon-neural tissuesDRG tissueCervical ganglionSciatic nervePolymerase chain reactionGanglion culturesAdducin geneLevel of expressionGangliaLow expression levelsGene expression
1999
Differential role of GDNF and NGF in the maintenance of two TTX-resistant sodium channels in adult DRG neurons
Fjell J, Cummins T, Dib-Hajj S, Fried K, Black J, Waxman S. Differential role of GDNF and NGF in the maintenance of two TTX-resistant sodium channels in adult DRG neurons. Brain Research 1999, 67: 267-282. PMID: 10216225, DOI: 10.1016/s0169-328x(99)00070-4.Peer-Reviewed Original ResearchMeSH KeywordsAge FactorsAnimalsAxotomyCell SizeCell SurvivalDown-RegulationDrug ResistanceFemaleGanglia, SpinalGene ExpressionGlial Cell Line-Derived Neurotrophic FactorLectinsMembrane PotentialsNAV1.8 Voltage-Gated Sodium ChannelNAV1.9 Voltage-Gated Sodium ChannelNerve Growth FactorsNerve Tissue ProteinsNeurons, AfferentNeuropeptidesPatch-Clamp TechniquesRatsRats, Sprague-DawleyRNA, MessengerSciatic NerveSodium ChannelsTetrodotoxinUp-RegulationConceptsTTX-R sodium currentsSNS/PN3Small DRG neuronsTTX-R currentsDRG neuronsIB4- neuronsSodium currentElectrophysiological propertiesSmall dorsal root ganglion neuronsDorsal root ganglion neuronsAxotomized DRG neuronsTTX-S currentsWhole-cell patch-clamp studiesTTX-resistant sodium channelsSciatic nerve transectionAdult DRG neuronsDifferent electrophysiological propertiesNear-normal levelsPatch-clamp studiesNerve transectionGDNF treatmentNeurotrophins NGFGanglion neuronsIsolectin IB4Exogenous NGF
1994
The expression of rat brain voltage-sensitive Na+ channel mRNAs in astrocytes
Oh Y, Black J, Waxman S. The expression of rat brain voltage-sensitive Na+ channel mRNAs in astrocytes. Brain Research 1994, 23: 57-65. PMID: 8028484, DOI: 10.1016/0169-328x(94)90211-9.Peer-Reviewed Original ResearchConceptsRat brainChannel mRNAChannel subtypesCultured spinal cordSkeletal muscleRat optic nerveNeuronal cell bodiesRegions of CNSSubtype IRat skeletal muscleOptic nervePolymerase chain reactionSpinal cordRat astrocytesDistinct subtypesAstrocytesCell bodiesSubtypesBrainRT-PCRSubtype IIRat tissuesChain reactionRat liverReverse transcription
1992
Chapter 8: The expression of sodium channels in astrocytes in situ and in vitro
Black J, Sontheimer H, Minturn J, Ransom B, Waxman S. Chapter 8: The expression of sodium channels in astrocytes in situ and in vitro. Progress In Brain Research 1992, 94: 89-107. PMID: 1337617, DOI: 10.1016/s0079-6123(08)61742-2.Peer-Reviewed Original ResearchConceptsOptic nerve astrocytesSodium channel expressionChannel expressionSodium channelsOptic nerveSodium current propertiesChannel expression patternsIon channel expressionSimilar electrophysiological propertiesCultured astrocytesAstrocytesElectrophysiological propertiesSodium currentHeterogeneous groupDifferent patternsNerveDifferent subpopulationsExpressionExpression patternsCell-cell interactionsHippocampusA2B5Neurons