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
2001
β1 adducin gene expression in DRG is developmentally regulated and is upregulated by glial-derived neurotrophic factor and nerve growth factor
Ghassemi F, Dib-Hajj S, Waxman S. β1 adducin gene expression in DRG is developmentally regulated and is upregulated by glial-derived neurotrophic factor and nerve growth factor. Brain Research 2001, 90: 118-124. PMID: 11406290, DOI: 10.1016/s0169-328x(01)00091-2.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCalmodulin-Binding ProteinsCells, CulturedCytoskeletonGanglia, SpinalGene Expression ProfilingGene Expression Regulation, DevelopmentalGlial Cell Line-Derived Neurotrophic FactorNerve Growth FactorNerve Growth FactorsNerve Tissue ProteinsNeurons, AfferentNeuroprotective AgentsRatsRats, Sprague-DawleyReverse Transcriptase Polymerase Chain ReactionConceptsGlial-derived neurotrophic factorReal-time reverse transcription-polymerase chain reactionNeurotrophic factorTrigeminal ganglionDRG culturesRat DRGGrowth factorDorsal root ganglion culturesAdult rat DRGRat dorsal root ganglion culturesSuperior cervical ganglionReverse transcription-polymerase chain reactionExpression levelsNerve growth factorNon-neural tissuesDRG tissueCervical ganglionSciatic nervePolymerase chain reactionGanglion culturesAdducin geneLevel of expressionGangliaLow expression levelsGene expression
1995
Endogenous GABA attenuates CNS white matter dysfunction following anoxia
Fern R, Waxman S, Ransom B. Endogenous GABA attenuates CNS white matter dysfunction following anoxia. Journal Of Neuroscience 1995, 15: 699-708. PMID: 7823173, PMCID: PMC6578328, DOI: 10.1523/jneurosci.15-01-00699.1995.Peer-Reviewed Original ResearchConceptsCompound action potentialEffect of GABAWhite matterEndogenous GABA releaseNerve fiber injuryGABA-B antagonistRelease of GABACAP recoveryGABA-B receptorsCNS white matterPertussis toxin treatmentWhite matter dysfunctionGABA-A agonistHigh agonist concentrationsReceptor/G-proteinControl conditionG proteinsPresence of GABAMin of anoxiaMM nipecotic acidFiber injuryGABA releaseReceptor blockadeOptic nerveEndogenous GABA