2024
TRPM8 Mutations Associated With Persistent Pain After Surgical Injury of Corneal Trigeminal Axons
Ghovanloo M, Effraim P, Tyagi S, Aldrich A, Cheng X, Yuan J, Schulman B, Jacobs D, Dib-Hajj S, Waxman S. TRPM8 Mutations Associated With Persistent Pain After Surgical Injury of Corneal Trigeminal Axons. Neurology Genetics 2024, 10: e200206. PMID: 39555137, PMCID: PMC11567650, DOI: 10.1212/nxg.0000000000200206.Peer-Reviewed Original ResearchLaser-assisted in situ keratomileusisPostoperative ocular painTrigeminal ganglion neuronsOcular painMultielectrode array recordingsPersistent painGanglion neuronsLaser-assisted in situ keratomileusis surgeryAxonal injuryRat trigeminal ganglion neuronsTransient receptor potential cation channelCorneal refractive surgeryMultielectrode arraysAnalysis of patientsPatch-clamp analysisGenomic analysis of patientsWild-typePatch-clamp resultsExposure to mentholRefractive surgeryHyperpolarizing directionNeuronal hyperexcitabilityPain-freeTrigeminal axonsWT channels
2023
Nav1.7 P610T mutation in two siblings with persistent ocular pain after corneal axon transection: impaired slow inactivation and hyperexcitable trigeminal neurons
Ghovanloo M, Effraim P, Yuan J, Schulman B, Jacobs D, Dib-Hajj S, Waxman S. Nav1.7 P610T mutation in two siblings with persistent ocular pain after corneal axon transection: impaired slow inactivation and hyperexcitable trigeminal neurons. Journal Of Neurophysiology 2023, 129: 609-618. PMID: 36722722, PMCID: PMC9988530, DOI: 10.1152/jn.00457.2022.Peer-Reviewed Original ResearchConceptsPersistent ocular painTrigeminal ganglion neuronsOcular painCorneal refractive surgeryGanglion neuronsRefractive surgeryAxonal injurySlow inactivationHuman pain modelTrigeminal afferent nervesTrigeminal ganglion axonsSmall subgroupPain-related disordersEffects of injurySodium channel Nav1.7Channel slow inactivationEye painPostoperative painMost patientsPain modelAfferent nervesPersistent painTrigeminal neuronsNav1.7 mutationAxon transection
2012
Axonal Protection with Sodium Channel Blocking Agents in Models of Multiple Sclerosis
Black J, Smith K, Waxman S. Axonal Protection with Sodium Channel Blocking Agents in Models of Multiple Sclerosis. 2012, 179-201. DOI: 10.1007/978-1-4614-2218-1_8.Peer-Reviewed Original ResearchExperimental autoimmune encephalomyelitisMultiple sclerosisSodium channelsAspects of MSAcute MS plaquesChronic inactive plaquesSignificant axonal damageImmune cell infiltrationSodium channel blockadeChannel Blocking AgentsSpinal cord axonsWhite matter axonsVoltage-gated sodium channelsAction potential conductionInactive plaquesClinical disabilityAutoimmune encephalomyelitisAxonal protectionNeuroinflammatory disordersNeurological deficitsNeuroprotective therapiesAxonal damageIschemia injuryAxonal degenerationAxonal injury
2005
29 Blocking the Axonal Injury Cascade Neuroprotection in Multiple Sclerosis and Its Models
Waxman S, Lo A. 29 Blocking the Axonal Injury Cascade Neuroprotection in Multiple Sclerosis and Its Models. 2005, 435-449. DOI: 10.1016/b978-012738761-1/50030-4.Peer-Reviewed Original ResearchExperimental autoimmune encephalomyelitisWhite matter injuryAxonal injuryChannel blockersNitric oxideNon-glucocorticoid steroidsCalcium channel blockersHuman multiple sclerosis lesionsSodium channel blockersMultiple sclerosis lesionsEffects of drugsAutoimmune encephalomyelitisMS pathologyOptic nerveMultiple sclerosisFunctional outcomeNeuroprotective agentsΓ-aminobutyric acidHypoxic injuryPathological evidenceSpinal nervesSpinal cordAdrenergic receptorsVivo preparationSclerosis lesions19 Molecular Mechanisms of Calcium Influx in Axonal Degeneration
Stys P, Waxman S. 19 Molecular Mechanisms of Calcium Influx in Axonal Degeneration. 2005, 275-292. DOI: 10.1016/b978-012738761-1/50020-1.Peer-Reviewed Original ResearchExperimental autoimmune encephalomyelitisAxonal degenerationMultiple sclerosisAxonal injuryCalcium influxInflammatory central nervous system disordersCentral nervous system disordersAcute axonal injuryPotential neuroprotective strategiesWhite matter injuryCellular calcium overloadNervous system disordersAutoimmune encephalomyelitisAxonal damageNeuroprotective strategiesGlutamate releasePathophysiological mechanismsCa overloadCalcium overloadSystem disordersInadequate deliveryMyelinated axonsAberrant operationNitric oxideCa channels
1999
The molecular pathophysiology of pain: abnormal expression of sodium channel genes and its contributions to hyperexcitability of primary sensory neurons
Waxman S. The molecular pathophysiology of pain: abnormal expression of sodium channel genes and its contributions to hyperexcitability of primary sensory neurons. Pain 1999, 82: s133-s140. PMID: 10491982, DOI: 10.1016/s0304-3959(99)00147-5.Peer-Reviewed Original ResearchConceptsPrimary sensory neuronsSodium channel gene expressionChannel gene expressionSodium channel expressionDRG neuronsSensory neuronsSodium channelsAxonal injuryChannel expressionSmall dorsal root ganglion neuronsAbnormal expressionDorsal root ganglion neuronsMolecular pathophysiologySodium channel geneAbnormal burst activityMultiple sodium channelsSNS/PN3Inflammatory pain modelChannel genesDistinct sodium channelsSodium current expressionInflammatory painNerve injuryPain modelGanglion neuronsChanges in expression of voltage‐gated potassium channels in dorsal root ganglion neurons following axotomy
Ishikawa K, Tanaka M, Black J, Waxman S. Changes in expression of voltage‐gated potassium channels in dorsal root ganglion neurons following axotomy. Muscle & Nerve 1999, 22: 502-507. PMID: 10204786, DOI: 10.1002/(sici)1097-4598(199904)22:4<502::aid-mus12>3.0.co;2-k.Peer-Reviewed Original ResearchConceptsDorsal root ganglion neuronsDRG neuronsVoltage-gated potassium channelsAxonal injuryGanglion neuronsPotassium channelsChannel expressionNormal DRG neuronsChronic pain syndromeSodium channel expressionSpectrum of subtypesVoltage-gated sodium channelsSpecific potassium channelsPain syndromeDRG cellsAdult ratsNervous systemAxotomyKv expressionNeuronsImmunocytochemical methodsMolecular correlatesElectrical excitabilitySodium channelsImmunoreactivity
1996
Mechanisms of Paresthesiae, Dysesthesiae, and Hyperesthesiae: Role of Na+ Channel Heterogeneity
Rizzo M, Kocsis J, Waxman S. Mechanisms of Paresthesiae, Dysesthesiae, and Hyperesthesiae: Role of Na+ Channel Heterogeneity. European Neurology 1996, 36: 3-12. PMID: 8719643, DOI: 10.1159/000117192.Peer-Reviewed Original ResearchConceptsAxonal injuryCutaneous afferentsDorsal root ganglion neuronsAction potential activityNormal sensory functionEctopic impulsesDRG neuronsClinical syndromeGanglion neuronsSensory functionMembrane excitabilityInjuryNerve impulsesDysesthesiaeChannel physiologyMolecular changesParesthesiaeAfferentsPreliminary evidenceNeuronsEctopicMolecular mechanismsSensory anatomyPotential activityPopulation
1995
Selective loss of slow and enhancement of fast Na+currents in cutaneous afferent dorsal root ganglion neurones following axotomy
Rizzo M, Kocsis J, Waxman S. Selective loss of slow and enhancement of fast Na+currents in cutaneous afferent dorsal root ganglion neurones following axotomy. Neurobiology Of Disease 1995, 2: 87-96. PMID: 8980012, DOI: 10.1006/nbdi.1995.0009.Peer-Reviewed Original Research
1994
Anoxic 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