2015
Comprehensive Corticospinal Labeling with mu-crystallin Transgene Reveals Axon Regeneration after Spinal Cord Trauma in ngr1−/− Mice
Fink KL, Strittmatter SM, Cafferty WB. Comprehensive Corticospinal Labeling with mu-crystallin Transgene Reveals Axon Regeneration after Spinal Cord Trauma in ngr1−/− Mice. Journal Of Neuroscience 2015, 35: 15403-15418. PMID: 26586827, PMCID: PMC4649010, DOI: 10.1523/jneurosci.3165-15.2015.Peer-Reviewed Original ResearchMeSH KeywordsAmidinesAnalysis of VarianceAnimalsAxonsBiotinCrystallinsDextransDisease Models, AnimalFunctional LateralityGene Expression RegulationGlial Fibrillary Acidic ProteinGPI-Linked ProteinsLuminescent ProteinsMiceMice, Inbred C57BLMice, TransgenicMu-CrystallinsMyelin ProteinsNerve RegenerationNogo Receptor 1Pyramidal TractsReceptors, Cell SurfaceRecovery of FunctionSpinal Cord InjuriesConceptsCorticospinal tractCST axonsTransgenic miceMotor tractsDextran amineFunctional deficitsSpinal cordAxon regenerationSpinal Cord Injury StudySpontaneous axon regenerationSpinal cord traumaNogo receptor 1Permanent functional deficitsPersistent functional deficitsBilateral pyramidotomyDorsal hemisectionMidthoracic cordCord traumaMotor pathwaysAdult CNSCST regenerationInjury studiesLesion siteRegenerating fibersNeural repair
2010
MAG and OMgp Synergize with Nogo-A to Restrict Axonal Growth and Neurological Recovery after Spinal Cord Trauma
Cafferty WB, Duffy P, Huebner E, Strittmatter SM. MAG and OMgp Synergize with Nogo-A to Restrict Axonal Growth and Neurological Recovery after Spinal Cord Trauma. Journal Of Neuroscience 2010, 30: 6825-6837. PMID: 20484625, PMCID: PMC2883258, DOI: 10.1523/jneurosci.6239-09.2010.Peer-Reviewed Original ResearchMeSH KeywordsAnalysis of VarianceAnimalsBiotinCells, CulturedDextransDisease Models, AnimalFemaleFunctional LateralityGanglia, SpinalGPI-Linked ProteinsMaleMiceMice, Inbred C57BLMice, KnockoutMutationMyelin ProteinsMyelin-Associated GlycoproteinMyelin-Oligodendrocyte GlycoproteinNerve Tissue ProteinsNeuronsNogo ProteinsPyramidal TractsReceptors, Cell SurfaceReceptors, SerotoninRecovery of FunctionSpinal Cord InjuriesConceptsAxonal growthSpinal Cord Injury StudyMutant miceGreater axonal growthGreater behavioral recoverySpinal cord traumaWild-type miceAxonal growth inhibitionHeterozygous mutant miceDeficient myelinNeurological recoveryCNS damageTriple-mutant miceBehavioral recoveryCord traumaFunctional recoveryNeurological functionMyelin inhibitorsAxonal regrowthReceptor mechanismsInjury studiesMyelin inhibitionDecoy receptorOptimal chanceMice
2007
Response to Correspondence: Kim et al., “Axon Regeneration in Young Adult Mice Lacking Nogo-A/B.” Neuron 38, 187–199
Cafferty WB, Kim JE, Lee JK, Strittmatter SM. Response to Correspondence: Kim et al., “Axon Regeneration in Young Adult Mice Lacking Nogo-A/B.” Neuron 38, 187–199. Neuron 2007, 54: 195-199. PMID: 17442242, PMCID: PMC2848952, DOI: 10.1016/j.neuron.2007.04.005.Peer-Reviewed Original Research
2005
Effect of combined treatment with methylprednisolone and soluble Nogo‐66 receptor after rat spinal cord injury
Ji B, Li M, Budel S, Pepinsky RB, Walus L, Engber TM, Strittmatter SM, Relton JK. Effect of combined treatment with methylprednisolone and soluble Nogo‐66 receptor after rat spinal cord injury. European Journal Of Neuroscience 2005, 22: 587-594. PMID: 16101740, PMCID: PMC2846292, DOI: 10.1111/j.1460-9568.2005.04241.x.Peer-Reviewed Original ResearchMeSH KeywordsAnalysis of VarianceAnimalsAxonsBehavior, AnimalBiotinCells, CulturedChick EmbryoDextransDisease Models, AnimalDose-Response Relationship, DrugDrug InteractionsDrug Therapy, CombinationExploratory BehaviorFemaleGanglia, SpinalGPI-Linked ProteinsImmunoglobulin GLaminectomyMethylprednisoloneMyelin ProteinsMyelin SheathNerve RegenerationNeuronsNogo Receptor 1Pyramidal TractsRatsRats, Long-EvansReceptors, Cell SurfaceReceptors, PeptideRecombinant ProteinsRecovery of FunctionSpinal Cord InjuriesConceptsSpinal cord injuryCord injuryRat spinal cord injuryMP treatmentAdult central nervous systemThoracic dorsal hemisectionNovel experimental therapiesCorticospinal tract axonsRecovery of functionNogo-66 receptorNumber of axonsCentral nervous systemGrowth inhibitory effectsDorsal hemisectionBBB scoresAxonal sproutingFunctional recoveryBresnahan (BBB) scoringAxonal regenerationMotor neuronsExperimental therapiesMethylprednisoloneSynthetic glucocorticoidNervous systemAxonal growth
2004
Neonatal hypoxia suppresses oligodendrocyte Nogo-A and increases axonal sprouting in a rodent model for human prematurity
Weiss J, Takizawa B, McGee A, Stewart WB, Zhang H, Ment L, Schwartz M, Strittmatter S. Neonatal hypoxia suppresses oligodendrocyte Nogo-A and increases axonal sprouting in a rodent model for human prematurity. Experimental Neurology 2004, 189: 141-149. PMID: 15296844, DOI: 10.1016/j.expneurol.2004.05.018.Peer-Reviewed Original ResearchMeSH KeywordsAge FactorsAnimalsAnimals, NewbornAxonsBehavior, AnimalBiotinCentral Nervous SystemDextransDisease Models, AnimalExploratory BehaviorHumansHypoxia, BrainImmunoblottingImmunohistochemistryInfant, NewbornInfant, PrematureMiceMice, Inbred C57BLMyelin Basic ProteinMyelin ProteinsMyelin-Associated GlycoproteinNogo ProteinsOligodendrogliaReceptors, Cell SurfaceTime FactorsConceptsChronic sublethal hypoxiaPeriventricular leukomalaciaMyelin associated glycoproteinCorticospinal tractWhite matterLow birth weight infantsCerebral white matter volumeBirth weight infantsLow birth weightAnterograde axonal tracingPeriventricular white matterPremature human infantsCNS white matterWhite matter volumeHypoxia-induced reductionWeight infantsAxonal sproutingCerebral ventriculomegalyCorticofugal fibersLocomotor hyperactivityNeonatal hypoxiaPersistent abnormalitiesMotor cortexBirth weightHuman prematurity