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