2024
Small fiber neuropathy
Kool D, Hoeijmakers J, Waxman S, Faber C. Small fiber neuropathy. International Review Of Neurobiology 2024 DOI: 10.1016/bs.irn.2024.10.001.Peer-Reviewed Original ResearchSmall fiber neuropathySodium channelopathiesAssociated with small fiber neuropathyTherapeutic strategiesNerve fibersNeuropathic pain disordersQuantitative sensory testingUnmyelinated C-fibersNervous systemSmall nerve fibersDiagnostic methodsPeripheral nervous systemAutonomic nervous systemNeuropathic painFiber neuropathyPain disordersClinical presentationC-fibersImmune-mediatedAutonomic dysfunctionClinical featuresSkin biopsiesDiagnosed patientsClinical trialsHereditary condition
2019
Rat NaV1.7 loss-of-function genetic model: Deficient nociceptive and neuropathic pain behavior with retained olfactory function and intra-epidermal nerve fibers
Grubinska B, Chen L, Alsaloum M, Rampal N, Matson D, Yang C, Taborn K, Zhang M, Youngblood B, Liu D, Galbreath E, Allred S, Lepherd M, Ferrando R, Kornecook T, Lehto S, Waxman S, Moyer B, Dib-Hajj S, Gingras J. Rat NaV1.7 loss-of-function genetic model: Deficient nociceptive and neuropathic pain behavior with retained olfactory function and intra-epidermal nerve fibers. Molecular Pain 2019, 15: 1744806919881846. PMID: 31550995, PMCID: PMC6831982, DOI: 10.1177/1744806919881846.Peer-Reviewed Original ResearchConceptsOlfactory functionNav1.7 proteinPain behaviorPain responseRat modelSmall-diameter dorsal root ganglion neuronsNormal intraepidermal nerve fibre densityIntraepidermal nerve fiber densityIntra-epidermal nerve fibersDorsal root ganglion neuronsNeuropathic pain behaviorsNeuropathic pain responsesSpinal nerve ligationNerve fiber densityDorsal root gangliaAction potential firingPeripheral nervous systemEarly postnatal developmentGenetic animal modelsNav1.7 lossNerve ligationPain targetsNeuropathic conditionsGanglion neuronsRoot ganglia
2016
Pharmacological reversal of a pain phenotype in iPSC-derived sensory neurons and patients with inherited erythromelalgia
Cao L, McDonnell A, Nitzsche A, Alexandrou A, Saintot PP, Loucif AJ, Brown AR, Young G, Mis M, Randall A, Waxman SG, Stanley P, Kirby S, Tarabar S, Gutteridge A, Butt R, McKernan RM, Whiting P, Ali Z, Bilsland J, Stevens EB. Pharmacological reversal of a pain phenotype in iPSC-derived sensory neurons and patients with inherited erythromelalgia. Science Translational Medicine 2016, 8: 335ra56. PMID: 27099175, DOI: 10.1126/scitranslmed.aad7653.Peer-Reviewed Original ResearchConceptsSensory neuronsPain conditionsSodium channelsClinical phenotypeSensory neuronal activityChronic pain conditionsHeat-induced painPeripheral nervous systemUnmet clinical needSodium channel Nav1.7Nav1.7 sodium channelNav1.7 blockersPharmacological reversalPain phenotypesExtreme painNeuronal activityHeat stimuliNervous systemChannel Nav1.7PainClinical needPatientsAberrant responsesSensory conditionsInduced pluripotent stem cell line
2000
Sensory neuron-specific sodium channel SNS is abnormally expressed in the brains of mice with experimental allergic encephalomyelitis and humans with multiple sclerosis
Black J, Dib-Hajj S, Baker D, Newcombe J, Cuzner M, Waxman S. Sensory neuron-specific sodium channel SNS is abnormally expressed in the brains of mice with experimental allergic encephalomyelitis and humans with multiple sclerosis. Proceedings Of The National Academy Of Sciences Of The United States Of America 2000, 97: 11598-11602. PMID: 11027357, PMCID: PMC17246, DOI: 10.1073/pnas.97.21.11598.Peer-Reviewed Original ResearchConceptsExperimental allergic encephalomyelitisMultiple sclerosisAllergic encephalomyelitisClinical abnormalitiesChannel expressionPurkinje cellsTrigeminal ganglion neuronsBrains of micePeripheral nervous systemSodium channel expressionIon channel expressionCerebellar Purkinje cellsAbnormal repertoiresAxonal degenerationControl miceGanglion neuronsControl subjectsMouse modelNormal brainAnimal modelsNervous systemNeurological diseasesSodium channelsProtein expressionAbnormal patterns
1999
Sodium channel expression in NGF‐overexpressing transgenic mice
Fjell J, Cummins T, Davis B, Albers K, Fried K, Waxman S, Black J. Sodium channel expression in NGF‐overexpressing transgenic mice. Journal Of Neuroscience Research 1999, 57: 39-47. PMID: 10397634, DOI: 10.1002/(sici)1097-4547(19990701)57:1<39::aid-jnr5>3.0.co;2-m.Peer-Reviewed Original ResearchConceptsNerve growth factorSodium channel expressionWild-type miceDRG neuronsTransgenic miceChannel expressionLevels of NGFDorsal root ganglion neuronsSNS/PN3Whole-cell patch-clamp studiesSmall DRG neuronsPeripheral nervous systemSodium channel mRNAFunctional sodium channelsPeak sodium current densityRegulation of expressionSodium current densityPatch-clamp studiesMechanical hyperalgesiaEmbryonic day 11Ganglion neuronsMouse DRGWild-type DRGsNervous systemLong-term overexpression
1995
Na+ channel β1 subunit mRNA: differential expression in rat spinal sensory neurons
Oh Y, Sashihara S, Black J, Waxman S. Na+ channel β1 subunit mRNA: differential expression in rat spinal sensory neurons. Brain Research 1995, 30: 357-361. PMID: 7637585, DOI: 10.1016/0169-328x(95)00052-t.Peer-Reviewed Original ResearchConceptsDRG neuronsNervous systemChannel beta 1 subunit (Na beta 1) mRNARat dorsal root ganglion neuronsCell bodiesDorsal root ganglion neuronsSubunit mRNAsBeta 1 mRNA expressionRat central nervous systemSmall DRG neuronsLarge DRG neuronsSpinal sensory neuronsPeripheral nervous systemPostnatal day 4Central nervous systemBeta 1 mRNABeta 1 subunit mRNASitu hybridization histochemistryAdult DRGGanglion neuronsSensory neuronsDay 4Hybridization histochemistryMRNA expressionNeuronsAnoxic/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 polarizationIschemiaDisease