2016
Early Activation of Experience-Independent Dendritic Spine Turnover in a Mouse Model of Alzheimer's Disease.
Heiss JK, Barrett J, Yu Z, Haas LT, Kostylev MA, Strittmatter SM. Early Activation of Experience-Independent Dendritic Spine Turnover in a Mouse Model of Alzheimer's Disease. Cerebral Cortex 2016, 27: 3660-3674. PMID: 27365298, PMCID: PMC6059166, DOI: 10.1093/cercor/bhw188.Peer-Reviewed Original ResearchMeSH KeywordsAge FactorsAlzheimer DiseaseAmyloid beta-Protein PrecursorAnalysis of VarianceAnimalsCerebral CortexDendritic SpinesDisease Models, AnimalGene Expression ProfilingGreen Fluorescent ProteinsHippocampusHumansImaging, Three-DimensionalImmunoprecipitationMiceMice, Inbred C57BLMice, TransgenicMutationNeuroimagingPlaque, AmyloidPresenilin-1Prion ProteinsProto-Oncogene Proteins c-fosSensory DeprivationTime FactorsVibrissaeConceptsAPP/PS1 miceDendritic spine turnoverSpine turnoverAlzheimer's diseasePS1 miceAged APP/PS1 miceYoung APP/PS1 miceAPP/PS1 mouse brainSoluble Aβ oligomersLipid-metabolizing genesAPPswe/Synaptic lossCerebral cortexSynapse densityAβ plaquesSynaptic dysregulationLack responsivenessMouse modelDendritic spinesPersistent spinesSynapse turnoverPlaque formationMouse brainYounger ageCellular prion protein
2015
Plasticity of Intact Rubral Projections Mediates Spontaneous Recovery of Function after Corticospinal Tract Injury
Siegel CS, Fink KL, Strittmatter SM, Cafferty WB. Plasticity of Intact Rubral Projections Mediates Spontaneous Recovery of Function after Corticospinal Tract Injury. Journal Of Neuroscience 2015, 35: 1443-1457. PMID: 25632122, PMCID: PMC4308593, DOI: 10.1523/jneurosci.3713-14.2015.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsDesigner DrugsFunctional LateralityGene Expression RegulationGlial Fibrillary Acidic ProteinLocomotionMaleMiceMice, Inbred C57BLMice, TransgenicMuscle StrengthMyelin ProteinsNeuronal PlasticityNogo ProteinsPsychomotor DisordersPyramidal TractsRaphe NucleiRecovery of FunctionSpinal Cord InjuriesStereotyped BehaviorTime FactorsConceptsSpinal cord injurySpontaneous functional recoveryFunctional recoverySpontaneous recoveryIncomplete spinal cord injuryCorticospinal tract lesionsWeeks of lesionCorticospinal tract injuryNogo receptor 1Nucleus raphe magnusTract injuryRubrospinal projectionsTract lesionsCord injuryRaphe magnusCircuit rearrangementsAdult CNSCircuit plasticityLocomotor functionAdult micePharmacogenetic toolsRed nucleusRubral projectionReceptor 1Extensive sprouting
2012
Limiting multiple sclerosis related axonopathy by blocking Nogo receptor and CRMP-2 phosphorylation
Petratos S, Ozturk E, Azari MF, Kenny R, Lee JY, Magee KA, Harvey AR, McDonald C, Taghian K, Moussa L, Aui P, Siatskas C, Litwak S, Fehlings MG, Strittmatter SM, Bernard CC. Limiting multiple sclerosis related axonopathy by blocking Nogo receptor and CRMP-2 phosphorylation. Brain 2012, 135: 1794-1818. PMID: 22544872, PMCID: PMC3589918, DOI: 10.1093/brain/aws100.Peer-Reviewed Original ResearchMeSH KeywordsAdultAnalysis of VarianceAnimalsAntibodiesAxonsCD3 ComplexCell Line, TumorDemyelinating DiseasesDisease Models, AnimalEncephalomyelitis, Autoimmune, ExperimentalFemaleGene Expression RegulationGlycoproteinsGPI-Linked ProteinsGreen Fluorescent ProteinsHumansImmunoprecipitationIntercellular Signaling Peptides and ProteinsMaleMiceMice, Inbred C57BLMice, KnockoutMiddle AgedMultiple SclerosisMutationMyelin ProteinsMyelin-Oligodendrocyte GlycoproteinNerve DegenerationNerve Tissue ProteinsNeuroblastomaNeurofilament ProteinsNogo Receptor 1Optic NervePeptide FragmentsPhosphorylationReceptors, Cell SurfaceRetinal Ganglion CellsSeverity of Illness IndexSilver StainingSpinal CordTau ProteinsTime FactorsTransduction, GeneticTubulinConceptsExperimental autoimmune encephalomyelitisAutoimmune encephalomyelitisMyelin oligodendrocyte glycoproteinMultiple sclerosisAxonal degenerationSpinal cordChronic active multiple sclerosis lesionsOptic nerve axonal degenerationNogo-66 receptor 1CRMP-2Axonal growth inhibitorsCollapsin response mediator protein 2Improved clinical outcomesSpinal cord neuronsRetinal ganglion cellsResponse mediator protein 2Central nervous systemViable therapeutic targetAdeno-associated viral vectorMultiple sclerosis lesionsClinical outcomesOptic nerveCord neuronsOligodendrocyte glycoproteinGanglion cells
2011
Recovery from chronic spinal cord contusion after nogo receptor intervention
Wang X, Duffy P, McGee AW, Hasan O, Gould G, Tu N, Harel NY, Huang Y, Carson RE, Weinzimmer D, Ropchan J, Benowitz LI, Cafferty WB, Strittmatter SM. Recovery from chronic spinal cord contusion after nogo receptor intervention. Annals Of Neurology 2011, 70: 805-821. PMID: 22162062, PMCID: PMC3238798, DOI: 10.1002/ana.22527.Peer-Reviewed Original ResearchConceptsChronic spinal cord injurySpinal cord injuryContusion injuryCord injurySpinal cord contusion injuryCentral nervous system injuryBresnahan locomotor scoresOpen-field BassoSpinal hemisection injuryWeight-bearing statusSpinal cord contusionMonths of treatmentNervous system injuryMyelin-derived inhibitorCaudal spinal cordPositron emission tomographyNgR1 pathwayRaphespinal axonsSpinal contusionCord contusionHemisection injuryFunctional recoveryLocomotor scoresSystem injuryControl rats
2009
Rho-Associated Kinase II (ROCKII) Limits Axonal Growth after Trauma within the Adult Mouse Spinal Cord
Duffy P, Schmandke A, Schmandke A, Sigworth J, Narumiya S, Cafferty WB, Strittmatter SM. Rho-Associated Kinase II (ROCKII) Limits Axonal Growth after Trauma within the Adult Mouse Spinal Cord. Journal Of Neuroscience 2009, 29: 15266-15276. PMID: 19955379, PMCID: PMC2855556, DOI: 10.1523/jneurosci.4650-09.2009.Peer-Reviewed Original ResearchMeSH KeywordsAmidesAnalysis of VarianceAnimalsAxonsBehavior, AnimalBrain InjuriesCA1 Region, HippocampalCells, CulturedCholera ToxinEnzyme InhibitorsGanglia, SpinalGene Expression RegulationMedian NeuropathyMiceMice, Inbred C57BLMice, KnockoutMyelin ProteinsNerve RegenerationNeuronsNogo ProteinsPyridinesReceptors, Calcitonin Gene-Related PeptideRhizotomyRho-Associated KinasesSpinal Cord InjuriesTime FactorsVersicansConceptsSpinal cordCNS traumaFunctional recoveryBasso Mouse Scale scoresSpinal Cord Injury StudyAxonal growthDorsal root entry zoneDorsal root ganglion neuronsAdult mouse spinal cordAxonal growth inhibitorsSpinal cord hemisectionRoot entry zoneSpinal cord injuryCaudal spinal cordMouse spinal cordDorsal hemisectionRaphespinal axonsDorsal rhizotomyCrush injuryCord hemisectionCorticospinal axonsChondroitin sulfate proteoglycanCord injuryGanglion neuronsInjury paradigmsFunctional outcome is impaired following traumatic brain injury in aging Nogo-A/B-deficient mice
Marklund N, Morales D, Clausen F, Hånell A, Kiwanuka O, Pitkänen A, Gimbel DA, Philipson O, Lannfelt L, Hillered L, Strittmatter SM, McIntosh TK. Functional outcome is impaired following traumatic brain injury in aging Nogo-A/B-deficient mice. Neuroscience 2009, 163: 540-551. PMID: 19555742, PMCID: PMC2756649, DOI: 10.1016/j.neuroscience.2009.06.042.Peer-Reviewed Original ResearchConceptsTraumatic brain injuryHemispheric tissue lossNeurological motor functionWT miceBrain injuryMotor functionCortical impact (CCI) TBILittermate controlsAge-matched wild-type littermate controlsMyelin stainingTissue lossMWM taskWild-type littermate controlsCortical lesion volumeAxonal growth inhibitorsRole of NogoMyelin-derived inhibitorAbsence of NogoNeurological motorPoor prognosisFunctional outcomeHemispheric tissuePathophysiological responsesWT littermatesDeficient mice
2006
Delayed Nogo receptor therapy improves recovery from spinal cord contusion
Wang X, Baughman KW, Basso DM, Strittmatter SM. Delayed Nogo receptor therapy improves recovery from spinal cord contusion. Annals Of Neurology 2006, 60: 540-549. PMID: 16958113, PMCID: PMC2855693, DOI: 10.1002/ana.20953.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAxonsDisease Models, AnimalDrug Administration ScheduleDrug Therapy, CombinationFemaleInjections, IntraventricularLocomotionMyelin SheathPhosphodiesterase InhibitorsPyramidal TractsRatsRats, Sprague-DawleyRecombinant Fusion ProteinsRecovery of FunctionRolipramSpinal Cord InjuriesTime FactorsTreatment OutcomeConceptsSpinal cord contusionCord contusionSpinal cordAxonal growthHuman spinal cord injuryAdult central nervous systemBresnahan locomotor scoresFc treatment groupVehicle-treated groupTime of injuryCyclic adenosine monophosphate phosphodiesterase inhibitorSpinal cord injuryRecovery of locomotionAddition of rolipramRostral spinal cordCentral nervous systemCaudal spinal cordBeneficial behavioral effectsDelayed therapyNeurological recoveryRaphespinal axonsAcute therapyCorticospinal axonsLocomotor scoresIntracerebroventricular route
2004
Nogo-66 Receptor Prevents Raphespinal and Rubrospinal Axon Regeneration and Limits Functional Recovery from Spinal Cord Injury
Kim JE, Liu BP, Park JH, Strittmatter SM. Nogo-66 Receptor Prevents Raphespinal and Rubrospinal Axon Regeneration and Limits Functional Recovery from Spinal Cord Injury. Neuron 2004, 44: 439-451. PMID: 15504325, DOI: 10.1016/j.neuron.2004.10.015.Peer-Reviewed Original ResearchMeSH Keywords5,7-DihydroxytryptamineAnimalsAxonsBehavior, AnimalBlotting, NorthernBlotting, SouthernBrainCell CountCells, CulturedCloning, MolecularCornified Envelope Proline-Rich ProteinsDesipramineDisease Models, AnimalEvoked Potentials, MotorFemaleGanglia, SpinalGlial Fibrillary Acidic ProteinGlucoseGPI-Linked ProteinsGrowth ConesImmunohistochemistryMiceMice, Inbred C57BLMice, KnockoutMotor ActivityMyelin ProteinsMyelin SheathMyelin-Associated GlycoproteinNerve RegenerationNeuronsNogo ProteinsNogo Receptor 1Phospholipid EthersProteinsPyramidal TractsReceptors, Cell SurfaceRecovery of FunctionSerotoninSerotonin AgentsSpinal CordSpinal Cord InjuriesTime FactorsConceptsAdult CNSNogo-66Spinal cord injuryAdult mammalian CNSNogo-66 receptorDorsal hemisectionDRG neuronsFunctional recoveryRubrospinal fibersCord injuryMyelin inhibitorsComplete transectionCorticospinal fibersMotor functionSpinal cordMotor impairmentAxon regenerationMammalian CNSAxonal growthAxonal outgrowthCNS myelinMiceInhibitory proteinInjuryGrowth conesNeonatal 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
1996
P2Y1 purinergic receptors in sensory neurons: contribution to touch-induced impulse generation.
Nakamura F, Strittmatter SM. P2Y1 purinergic receptors in sensory neurons: contribution to touch-induced impulse generation. Proceedings Of The National Academy Of Sciences Of The United States Of America 1996, 93: 10465-10470. PMID: 8816824, PMCID: PMC38408, DOI: 10.1073/pnas.93.19.10465.Peer-Reviewed Original ResearchMeSH KeywordsAdenosine TriphosphateAnimalsApyraseChickensFemaleGanglia, SpinalMembrane PotentialsMolecular Sequence DataNerve FibersNeurons, AfferentOocytesPhysical StimulationPurinergic P2 Receptor AgonistsPyridoxal PhosphateRatsReceptors, Purinergic P2Receptors, Purinergic P2X3Receptors, Purinergic P2Y1RNA, MessengerSciatic NerveSkinSuraminTime FactorsTranscription, GeneticXenopus laevisConceptsNerve endingsPurinergic receptorsSensory neuronsAction potentialsSmall fiber sensory neuronsDorsal root ganglion neuronsDistal nerve endingsSensory action potentialsPeripheral nerve endingsSensory nerve fibersP2 receptor agonistsP2Y1 purinergic receptorRelease of ATPP2 antagonistsGanglion neuronsReceptor agonistNerve fibersLight touchNeuronsXenopus laevis oocytesSomatic sensationsReceptorsImpulse generationExtracellular spaceLaevis oocytes
1986
Angiotensin-Converting Enzyme Localized in the Rat Pituitary and Adrenal Glands by [3H]Captopril Autoradiography*
STRITTMATTER S, DE SOUZA E, LYNCH D, SNYDER S. Angiotensin-Converting Enzyme Localized in the Rat Pituitary and Adrenal Glands by [3H]Captopril Autoradiography*. Endocrinology 1986, 118: 1690-1699. PMID: 3004925, DOI: 10.1210/endo-118-4-1690.Peer-Reviewed Original ResearchConceptsFmol/Adrenal medullaReserpine treatmentAdrenal glandAnterior pituitaryAngiotensin-converting enzymeRat pituitary glandAngiotension-converting enzymeAdrenal cortexDexamethasone treatmentPituitary glandPosterior pituitaryBrattleboro ratsMedullaBovine adrenal medullaPituitaryRatsIntermediate pituitaryGlandHypophysectomyAutoradiographyTreatmentChromaffin granulesAdrenalectomyAngiotensin