2023
Inflammation differentially controls transport of depolarizing Nav versus hyperpolarizing Kv channels to drive rat nociceptor activity
Higerd-Rusli G, Tyagi S, Baker C, Liu S, Dib-Hajj F, Dib-Hajj S, Waxman S. Inflammation differentially controls transport of depolarizing Nav versus hyperpolarizing Kv channels to drive rat nociceptor activity. Proceedings Of The National Academy Of Sciences Of The United States Of America 2023, 120: e2215417120. PMID: 36897973, PMCID: PMC10089179, DOI: 10.1073/pnas.2215417120.Peer-Reviewed Original ResearchConceptsCell biological mechanismsAxonal surfaceLive-cell imagingIon channel traffickingAnterograde transport vesiclesTransport vesiclesInflammatory mediatorsChannel traffickingPlasma membraneVesicular loadingIon channelsKv channelsPotential therapeutic targetPotassium channel KSodium channel NaTraffickingBiological mechanismsTherapeutic targetAbundanceRetrograde transportDistal axonsChannel NaInflammatory painNociceptor activityAxonal transport
2014
Dynamics of sodium channel Nav1.5 expression in astrocytes in mouse models of multiple sclerosis
Pappalardo LW, Liu S, Black JA, Waxman SG. Dynamics of sodium channel Nav1.5 expression in astrocytes in mouse models of multiple sclerosis. Neuroreport 2014, 25: 1208-1215. PMID: 25144393, PMCID: PMC4159404, DOI: 10.1097/wnr.0000000000000249.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAstrocytesEncephalomyelitis, Autoimmune, ExperimentalImmunohistochemistryLumbar VertebraeMice, BiozziMice, Inbred C57BLMotor CortexMultiple Sclerosis, Chronic ProgressiveMultiple Sclerosis, Relapsing-RemittingNAV1.5 Voltage-Gated Sodium ChannelSeverity of Illness IndexSpinal CordUp-RegulationConceptsExperimental autoimmune encephalomyelitisCentral nervous systemMultiple sclerosisNervous systemChronic multiple sclerosis lesionsNav1.5 expressionPhases of relapsePeriods of remissionGlial scar formationResponse of astrocytesSeverity of diseasePotential therapeutic targetMultiple sclerosis lesionsVoltage-gated sodium channel Nav1.5Autoimmune encephalomyelitisNeuroinflammatory pathologiesIntracellular Ca levelsReactive astrogliosisGlial scarInflammatory pathologyMouse modelImmunohistochemical analysisScar formationTherapeutic targetAstrocytes