2025
Optic nerve injury impairs intrinsic mechanisms underlying electrical activity in a resilient retinal ganglion cell
Zapadka T, Tran N, Demb J. Optic nerve injury impairs intrinsic mechanisms underlying electrical activity in a resilient retinal ganglion cell. The Journal Of Physiology 2025 PMID: 39985791, DOI: 10.1113/jp286414.Peer-Reviewed Original ResearchOptic nerve crushRetinal ganglion cellsOptic nerveGanglion cellsSynaptic inputsVoltage-gated sodium channel currentsRetinal ganglion cell typesVoltage-gatedRetinal ganglion cell survivalChelation of intracellular calciumResting membrane potentialOptic nerve injuryVoltage-gated currentsAxonal injurySodium channel currentsRetinal ganglion cell axonsRGC typesAlpha retinal ganglion cellsAxon initial segmentIntracellular calciumRate of survivalNerve injuryElectrophysiological propertiesNerve crushIntrinsic excitability
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
2015
Absence of Cerebrospinal Fluid Signs of Neuronal Injury Before and After Immediate Antiretroviral Therapy in Acute HIV Infection
Peluso MJ, Valcour V, Ananworanich J, Sithinamsuwan P, Chalermchai T, Fletcher JL, Lerdlum S, Chomchey N, Slike B, Sailasuta N, Gisslén M, Zetterberg H, Spudich S, Teams O. Absence of Cerebrospinal Fluid Signs of Neuronal Injury Before and After Immediate Antiretroviral Therapy in Acute HIV Infection. The Journal Of Infectious Diseases 2015, 212: 1759-1767. PMID: 25995196, PMCID: PMC4633761, DOI: 10.1093/infdis/jiv296.Peer-Reviewed Original ResearchConceptsCombination antiretroviral therapyAcute HIV infectionCSF NfL levelsNeurofilament light chainChronic HIV infectionHIV infectionNfL levelsParietal gray matterFrontal white matterNeuronal injuryAcute infectionGray matterCART initiationAntiretroviral therapyAcute human immunodeficiency virus (HIV) infectionCerebrospinal fluid neurofilament light chainProton magnetic resonance spectroscopic findingsWhite matterHuman immunodeficiency virus (HIV) infectionN-acetylaspartate/creatineMagnetic resonance spectroscopic findingsImmediate antiretroviral therapyImmunodeficiency virus infectionFrontal gray matterAxonal injuryNeuropathology of Traumatic Brain Injury: Comparison of Penetrating, Nonpenetrating Direct Impact and Explosive Blast Etiologies
de Lanerolle NC, Kim JH, Bandak FA. Neuropathology of Traumatic Brain Injury: Comparison of Penetrating, Nonpenetrating Direct Impact and Explosive Blast Etiologies. Seminars In Neurology 2015, 35: 012-019. PMID: 25714863, DOI: 10.1055/s-0035-1544240.Peer-Reviewed Original ResearchConceptsClosed head injuryTraumatic brain injuryDiffuse axonal injuryAxonal injuryMild TBIHead injuryBrain injurySevere closed head injuryModerate traumatic brain injuryModerate closed head injuryMild traumatic brain injuryAnimal TBI modelsMicroglial activationNeuronal injuryTBI modelCerebral vasculatureInjuryNeuropathologyGross disruptionHuman brainBlunt impactUnique patternHumansActivationAstrocytes
2013
Sodium Channels Contribute to Degeneration of Dorsal Root Ganglion Neurites Induced by Mitochondrial Dysfunction in an In Vitro Model of Axonal Injury
Persson AK, Kim I, Zhao P, Estacion M, Black JA, Waxman SG. Sodium Channels Contribute to Degeneration of Dorsal Root Ganglion Neurites Induced by Mitochondrial Dysfunction in an In Vitro Model of Axonal Injury. Journal Of Neuroscience 2013, 33: 19250-19261. PMID: 24305821, PMCID: PMC6618782, DOI: 10.1523/jneurosci.2148-13.2013.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAxonsAxotomyCell DeathCells, CulturedGanglia, SpinalHumansHydrogen PeroxideImmunohistochemistryMiceMice, TransgenicMicrotubulesMitochondrial DiseasesNerve DegenerationNeuritesOxidantsRotenoneSodium Channel BlockersSodium ChannelsSodium-Calcium ExchangerSodium-Potassium-Exchanging ATPaseTetrodotoxinThioureaUncoupling AgentsConceptsAxonal degenerationNeurite degenerationSodium channelsKB-R7943Mouse peripheral sensory neuronsRotenone-induced mitochondrial dysfunctionOxidative stressMitochondrial dysfunctionPeripheral sensory neuronsDorsal root gangliaPeripheral nervous systemDegeneration of neuritesMitochondrial functionVoltage-gated sodium channelsMultiple neurodegenerative disordersSodium-calcium exchangerImpaired mitochondrial functionInjurious cascadeAxonal injuryActivity blockadeRoot gangliaAxonal neuropathySensory neuronsNCX activityDysfunctional intracellularSuppression of Inflammatory Responses during Myelin Oligodendrocyte Glycoprotein–Induced Experimental Autoimmune Encephalomyelitis Is Regulated by AKT3 Signaling
Tsiperson V, Gruber R, Goldberg M, Jordan A, Weinger J, Macian F, Shafit-Zagardo B. Suppression of Inflammatory Responses during Myelin Oligodendrocyte Glycoprotein–Induced Experimental Autoimmune Encephalomyelitis Is Regulated by AKT3 Signaling. The Journal Of Immunology 2013, 190: 1528-1539. PMID: 23335751, PMCID: PMC3564598, DOI: 10.4049/jimmunol.1201387.Peer-Reviewed Original ResearchMeSH KeywordsAcute DiseaseAnimalsChronic DiseaseEncephalomyelitis, Autoimmune, ExperimentalGenetic Predisposition to DiseaseInflammation MediatorsLumbosacral RegionMaleMiceMice, Inbred C57BLMice, KnockoutMyelin-Oligodendrocyte GlycoproteinPeptide FragmentsProto-Oncogene Proteins c-aktSeverity of Illness IndexSignal TransductionSpinal CordConceptsExperimental autoimmune encephalomyelitisSpinal cordAutoimmune encephalomyelitisWT miceImmune cellsBone marrow-derived immune cellsRegulatory T cell-mediated suppressionAcute experimental autoimmune encephalomyelitisT cell-mediated suppressionWT spinal cordsRegulatory T cellsBone marrow chimerasCell-mediated suppressionProtection of miceMyelin oligodendrocyte glycoproteinWild-type miceIFN-γ mRNABone marrow cellsAkt3 signalingMore demyelinationQuantitative RT-PCRCNS damageIL-17Axonal injuryClinical scores
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
2011
Characteristics of an Explosive Blast-Induced Brain Injury in an Experimental Model
de Lanerolle NC, Bandak F, Kang D, Li AY, Du F, Swauger P, Parks S, Ling G, Kim JH. Characteristics of an Explosive Blast-Induced Brain Injury in an Experimental Model. Journal Of Neuropathology & Experimental Neurology 2011, 70: 1046-1057. PMID: 22002430, DOI: 10.1097/nen.0b013e318235bef2.Peer-Reviewed Original ResearchConceptsBrain injuryAxonal injuryΒ-amyloid precursor protein immunohistochemistryAnesthetized Yorkshire swineBlast-Induced Brain InjuryMild traumatic brain injuryPrecursor protein immunohistochemistryTraumatic brain injuryBlast injury modelAstrocyte activationNeuronal injuryNeuropathologic changesIntracranial hemorrhageNeuropathologic consequencesProtein immunohistochemistryHistologic changesNeurobehavioral outcomesInjury modelPathologic changesSham controlsMood disordersInjuryYorkshire swineExperimental modelHuman brain
2009
Dysmyelinated axons in shiverer mice are highly vulnerable to α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptor-mediated toxicity
Pitt D, Gonzales E, Cross AH, Goldberg MP. Dysmyelinated axons in shiverer mice are highly vulnerable to α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptor-mediated toxicity. Brain Research 2009, 1309: 146-154. PMID: 19896473, PMCID: PMC7343376, DOI: 10.1016/j.brainres.2009.10.066.Peer-Reviewed Original ResearchMeSH Keywordsalpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic AcidAnimalsBiomarkersBrainDisease Models, AnimalExcitatory Amino Acid AgonistsFemaleHereditary Central Nervous System Demyelinating DiseasesLuminescent ProteinsMiceMice, Inbred C57BLMice, Neurologic MutantsMovement DisordersMyelin Basic ProteinN-MethylaspartateNerve DegenerationNerve Fibers, MyelinatedNeurotoxinsReceptors, AMPAConceptsNMDA receptorsShiverer miceAMPA/kainate receptorsLumbar dorsal columnWhite matter injuryWidespread axonal degenerationSpinal cord axonsActivation of receptorsReceptor-mediated toxicitySubset of axonsMyelin basic proteinAxonal vulnerabilityNeuroprotective therapiesGlutamate excitotoxicityNMDA injectionAxonal degenerationAxonal injuryDorsal columnsRotarod performanceAxon damageGlutamate toxicityCentral axonsGlial cellsS-AMPAAxonal toxicityContribution of White Matter Lesions to Gray Matter Atrophy in Multiple Sclerosis: Evidence From Voxel-Based Analysis of T1 Lesions in the Visual Pathway
Sepulcre J, Goñi J, Masdeu J, Bejarano B, de Mendizábal N, Toledo J, Villoslada P. Contribution of White Matter Lesions to Gray Matter Atrophy in Multiple Sclerosis: Evidence From Voxel-Based Analysis of T1 Lesions in the Visual Pathway. JAMA Neurology 2009, 66: 173-179. PMID: 19204153, DOI: 10.1001/archneurol.2008.562.Peer-Reviewed Original ResearchConceptsLateral geniculate nucleus atrophyGM atrophyMultiple sclerosisOptic pathway lesionsOptical radiationWhite matterOptic radiation lesionsGray matterWM regionsRegional GM atrophyWhite matter lesionsLesion probability mapsVoxel-based analysisT1 lesionsPathway lesionsLateral geniculate nucleusRadiation lesionsPresence of lesionsMultiple Sclerosis CenterGray matter atrophyOptic pathwayMultiple sclerosis plaquesAtrophyLesionsAxonal injury
2005
Electrophysiological properties of two axonal sodium channels, Nav1.2 and Nav1.6, expressed in mouse spinal sensory neurones
Rush AM, Dib‐Hajj S, Waxman SG. Electrophysiological properties of two axonal sodium channels, Nav1.2 and Nav1.6, expressed in mouse spinal sensory neurones. The Journal Of Physiology 2005, 564: 803-815. PMID: 15760941, PMCID: PMC1464456, DOI: 10.1113/jphysiol.2005.083089.Peer-Reviewed Original Research29 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
2004
Diffusion tensor imaging as potential biomarker of white matter injury in diffuse axonal injury.
Huisman T, Schwamm L, Schaefer P, Koroshetz W, Shetty-Alva N, Ozsunar Y, Wu O, Sorensen A. Diffusion tensor imaging as potential biomarker of white matter injury in diffuse axonal injury. American Journal Of Neuroradiology 2004, 25: 370-6. PMID: 15037457, PMCID: PMC8158566.Peer-Reviewed Original ResearchConceptsGlasgow Coma ScaleDiffusion tensor imagingTraumatic brain injuryRankin scoreInternal capsuleApparent diffusion coefficientADC valuesFA valuesWhite matter injuryHealthy control subjectsDiffuse axonal injuryCorresponding ADC valuesFractional anisotropy valuesNew MR imaging techniquesTBI correlatesComa ScaleClinical scoresAxonal injuryControl subjectsBrain injuryClinical markersMR imaging techniquesTissue injuryBrain ultrastructureWhite matter
2003
Delayed Systemic Nogo-66 Receptor Antagonist Promotes Recovery from Spinal Cord Injury
Li S, Strittmatter SM. Delayed Systemic Nogo-66 Receptor Antagonist Promotes Recovery from Spinal Cord Injury. Journal Of Neuroscience 2003, 23: 4219-4227. PMID: 12764110, PMCID: PMC6741116, DOI: 10.1523/jneurosci.23-10-04219.2003.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceAnimalsAxonsAxotomyBehavior, AnimalCornified Envelope Proline-Rich ProteinsFemaleGanglia, SpinalGPI-Linked ProteinsInjections, SubcutaneousIntralaminar Thalamic NucleiMembrane ProteinsMiceMice, Inbred C57BLMolecular Sequence DataMolecular WeightMotor ActivityMyelin ProteinsNerve FibersNerve RegenerationNogo Receptor 1Peptide FragmentsProtein BiosynthesisProteinsPyramidal TractsReceptors, Cell SurfaceSerotoninSpinal CordSpinal Cord InjuriesConceptsSpinal cord injuryCord injuryCorticospinal axonsThoracic spinal cord injuryTherapeutic time windowSpinal cord hemisectionSpinal cord traumaCorticospinal tract axonsAdult mammalian CNSNogo-66 receptorOligodendrocyte myelin glycoproteinCNS axonal injuryCord lesionsSubcutaneous treatmentSystemic therapyCord hemisectionCord traumaIntrathecal applicationLocal therapyLocomotor recoveryFunctional recoverySerotonergic fibersAxonal injuryReceptor antagonistAxon sprouting
1999
Molecular pathogenesis of multiple sclerosis
Bar-Or A, Oliveira E, Anderson D, Hafler D. Molecular pathogenesis of multiple sclerosis. Journal Of Neuroimmunology 1999, 100: 252-259. PMID: 10695735, DOI: 10.1016/s0165-5728(99)00193-9.Peer-Reviewed Original ResearchConceptsMultiple sclerosisT cellsMyelin-reactive T cellsCentral nervous system white matterB7 costimulatory pathwayNervous system white matterDifferential activation statesMacrophage infiltratesMS patientsAxonal injuryNeurological functionProinflammatory cellsProinflammatory cytokinesCostimulatory pathwayInflammatory diseasesMS lesionsMolecular pathogenesisWhite matterMolecular mimicryMatrix metalloproteinasesNormal individualsAdhesion moleculesSelective expressionSclerosisActivation stateThe 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
Chapter 8 Alterations in the functional properties of dorsal root ganglion cells with unmyelinated axons after a chronic nerve constriction in the rat
LaMotte R, Zhang J, Petersen M. Chapter 8 Alterations in the functional properties of dorsal root ganglion cells with unmyelinated axons after a chronic nerve constriction in the rat. Progress In Brain Research 1996, 110: 105-111. PMID: 9000719, DOI: 10.1016/s0079-6123(08)62568-6.Peer-Reviewed Original ResearchConceptsDorsal root gangliaSensory neuronsIntact neuronsPartial peripheral nerve injuryDorsal root ganglion cellsChronic nerve constrictionPeripheral axonal injuryPeripheral nerve injuryPeripheral sensory neuronsPrimary sensory neuronsNerve constrictionNerve injuryAbnormal responsivenessAxonal injuryCollateral sproutingNeuropathological changesNociceptive activityDRG cellsRoot gangliaGanglion cellsSame nerveInjury siteUnmyelinated axonsAxonsNeurons
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