2024
Nav1.7 as a chondrocyte regulator and therapeutic target for osteoarthritis
Fu W, Vasylyev D, Bi Y, Zhang M, Sun G, Khleborodova A, Huang G, Zhao L, Zhou R, Li Y, Liu S, Cai X, He W, Cui M, Zhao X, Hettinghouse A, Good J, Kim E, Strauss E, Leucht P, Schwarzkopf R, Guo E, Samuels J, Hu W, Attur M, Waxman S, Liu C. Nav1.7 as a chondrocyte regulator and therapeutic target for osteoarthritis. Nature 2024, 625: 557-565. PMID: 38172636, PMCID: PMC10794151, DOI: 10.1038/s41586-023-06888-7.Peer-Reviewed Original ResearchVoltage-gated sodium channelsOA progressionDorsal root ganglion neuronsStructural joint damagePain relief treatmentHuman OA chondrocytesCommon joint diseaseMultiple mouse modelsNav1.7 blockersPain behaviorGanglion neuronsPharmacological blockadeJoint damageJoint degenerationChannel blockersJoint diseaseOA chondrocytesMouse modelTherapeutic targetOsteoarthritisIntracellular Ca2Nav1.7Nav1.7 channelsGenetic ablationLimited evidence
2019
Sodium Channels and Pain
Cummins T, Waxman S, Wood J. Sodium Channels and Pain. 2019, 233-262. DOI: 10.1093/oxfordhb/9780190860509.013.3.Peer-Reviewed Original ResearchSodium channel blockersPain conditionsChannel blockersSodium channelsAnalgesic drug targetsDifferent pain statesFunction Nav1.7 mutationsMost pain conditionsPeripheral sodium channelsSodium channel subtypesDamage-sensing neuronsDrug developmentVoltage-gated sodium channelsSodium channel isoformsDrug development programsIon channelsExcellent analgesicPain controlPain reliefPain statesNav1.7 mutationSodium-selective ion channelsNew analgesicsLocal anestheticsTherapeutic approaches
2008
Mechanisms of Disease: sodium channels and neuroprotection in multiple sclerosis—current status
Waxman SG. Mechanisms of Disease: sodium channels and neuroprotection in multiple sclerosis—current status. Nature Reviews Neurology 2008, 4: 159-169. PMID: 18227822, DOI: 10.1038/ncpneuro0735.Peer-Reviewed Original Research
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 lesions
1999
The role of voltage-gated Ca2+ channels in anoxic injury of spinal cord white matter
Imaizumi T, Kocsis J, Waxman S. The role of voltage-gated Ca2+ channels in anoxic injury of spinal cord white matter. Brain Research 1999, 817: 84-92. PMID: 9889329, DOI: 10.1016/s0006-8993(98)01214-1.Peer-Reviewed Original ResearchConceptsVoltage-gated Ca2Spinal cord axonsAnoxic injuryDorsal columnsR-type voltage-gated Ca2N-type calcium channelsSpinal cord white matterRat dorsal columnsDorsal column axonsR-type Ca2Rat spinal cordCord white matterT-type channelsInflux of Ca2Dose-dependent mannerLoss of conductionAxonal conductionSpinal cordChannel blockersCalcium channelsSurface stimulationWhite matterPerfusion solutionInjuryGlass microelectrodes
1992
Ionic mechanisms of anoxic injury in mammalian CNS white matter: role of Na+ channels and Na(+)-Ca2+ exchanger
Stys P, Waxman S, Ransom B. Ionic mechanisms of anoxic injury in mammalian CNS white matter: role of Na+ channels and Na(+)-Ca2+ exchanger. Journal Of Neuroscience 1992, 12: 430-439. PMID: 1311030, PMCID: PMC6575619, DOI: 10.1523/jneurosci.12-02-00430.1992.Peer-Reviewed Original ResearchConceptsRat optic nerveCompound action potentialAnoxic injuryOptic nerveWhite matterAction potentialsCentral white matter tractsWhite matter injuryCNS white matterMembrane depolarizationAnoxia/ischemiaWhite matter tractsCNS protectionAnoxic insultMyelinated tractsChannel blockersExchanger blockerIrreversible injuryExtracellular Ca2Mammalian CNSNerveInjuryMore injuriesBlockersFunctional integrity
1990
Effects of polyvalent cations and dihydropyridine calcium channel blockers on recovery of CNS white matter from anoxia
Stys P, Ransom B, Waxman S. Effects of polyvalent cations and dihydropyridine calcium channel blockers on recovery of CNS white matter from anoxia. Neuroscience Letters 1990, 115: 293-299. PMID: 2234507, DOI: 10.1016/0304-3940(90)90471-k.Peer-Reviewed Original ResearchConceptsAnoxic injuryChannel blockersWhite matterMammalian central white matterDihydropyridine calcium channel blockerChannel blockers Mn2Irreversible anoxic injuryCalcium channel blockersCNS white matterCompound action potentialCentral white matterDihydropyridine classOrganic Ca2Inorganic Ca2Extracellular Ca2Action potentialsNerve modelMin periodBlockersInjuryFunctional integrityConventional Ca2Ca2InfluxIntracellular compartments
1989
Pharmacological sensitivities of two afterhyperpolarizations in rat optic nerve
Gordon T, Kocsis J, Waxman S. Pharmacological sensitivities of two afterhyperpolarizations in rat optic nerve. Brain Research 1989, 502: 252-257. PMID: 2555026, DOI: 10.1016/0006-8993(89)90620-3.Peer-Reviewed Original ResearchConceptsRat optic nerveOptic nerveEarly afterhyperpolarizationPharmacological sensitivityAction potentialsPeak latencyAction potential broadeningConstant current depolarizationSucrose gap chamberPotassium channel blockerLate afterhyperpolarizationChannel blockersRepetitive stimulationAfterhyperpolarizationNervePotassium conductanceSucrose gapTetraethylammoniumPotential broadeningCurrent depolarizationDepolarizationDurationApaminBlockersCharybdotoxin