2001
Acquired channelopathies in nerve injury and MS
Waxman S. Acquired channelopathies in nerve injury and MS. Neurology 2001, 56: 1621-1627. PMID: 11428390, DOI: 10.1212/wnl.56.12.1621.Peer-Reviewed Original ResearchConceptsNerve injurySodium channelsSensory neuron-specific sodium channelsSodium channel geneChannel genesPeripheral nerve injurySpinal sensory neuronsPathophysiology of MSSubtype-specific drugsDistinct sodium channelsVoltage-gated sodium channelsSpecific sodium channelsAxonal transectionGenetic channelopathyPrototype disorderSensory neuronsPurkinje cellsTherapeutic opportunitiesChannelopathiesAbnormal expressionInjuryMolecular changesHyperexcitabilityCellsTransection
2000
The neuron as a dynamic electrogenic machine: modulation of sodiumchannel expression as a basis for functional plasticity in neurons
Waxman S. The neuron as a dynamic electrogenic machine: modulation of sodiumchannel expression as a basis for functional plasticity in neurons. Philosophical Transactions Of The Royal Society B Biological Sciences 2000, 355: 199-213. PMID: 10724456, PMCID: PMC1692729, DOI: 10.1098/rstb.2000.0559.Peer-Reviewed Original ResearchConceptsSodium channelsMammalian nervous systemSodium channel geneNervous systemDozen genesDistinct sodium channelsVoltage-gated sodium channelsGenesElectrogenic machineryNormal nervous systemSodium channel expressionFunctional plasticityMembrane of neuronsAction potential activityTranscriptionPathological insultsPhysiological inputsMost neuronsCrucial roleExpressionNeuronsFunctional propertiesElectroresponsive propertiesPotential activityMachinery
1999
Sodium channels, excitability of primary sensory neurons, and the molecular basis of pain
Waxman S, Cummins T, Dib‐Hajj S, Fjell J, Black J. Sodium channels, excitability of primary sensory neurons, and the molecular basis of pain. Muscle & Nerve 1999, 22: 1177-1187. PMID: 10454712, DOI: 10.1002/(sici)1097-4598(199909)22:9<1177::aid-mus3>3.0.co;2-p.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsPrimary sensory neuronsDRG neuronsSodium channel expressionSodium channel gene expressionSensory neuronsChannel gene expressionSodium channelsChannel expressionSodium currentTTX-sensitive sodium currentAbnormal burst activityNormal DRG neuronsSNS/PN3Resistant sodium currentsDistinct sodium channelsSodium channel geneChannel genesInflammatory painNerve injuryAxonal transectionElectrophysiological abnormalitiesSelective blockadePharmacological approachesBurst activityPainThe 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 neurons