0000000000202418

AUTHOR

David H. Rowitch

0000-0002-0079-0060

showing 3 related works from this author

Extensive migration of young neurons into the infant human frontal lobe

2016

Building the human brain As the brain develops, neurons migrate from zones of proliferation to their final locations, where they begin to build circuits. Paredes et al. have discovered that shortly after birth, a group of neurons that proliferates near the ventricles migrates in chains alongside circulatory vessels into the frontal lobes (see the Perspective by McKenzie and Fishell). Young neurons that migrate postnatally into the anterior cingulate cortex then develop features of inhibitory interneurons. The number of migratory cells decreases over the first 7 months of life, and by 2 years of age, migratory cells are not evident. Any damage during migration, such as hypoxia, may affect th…

Doublecortin Domain Proteins0301 basic medicineNeurogenesisNeuropeptideBiologyInhibitory postsynaptic potentialGyrus Cinguli03 medical and health sciencesLateral ventricles0302 clinical medicineCell MovementInterneuronsLateral VentriclesCorrespondenceNeuroplasticitymedicineHumansGyrus cinguliAnterior cingulate cortexNeuronsNeuronal PlasticityMultidisciplinaryNeuropeptidesNeurogenesisInfantAnatomyFrontal Lobe030104 developmental biologymedicine.anatomical_structureFrontal lobeMicrotubule-Associated Proteins030217 neurology & neurosurgeryScience
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Wnt-Dependent Oligodendroglial-Endothelial Interactions Regulate White Matter Vascularization and Attenuate Injury

2020

Recent studies have indicated oligodendroglial-vascular crosstalk during brain development, but the underlying mechanisms are incompletely understood. We report that oligodendrocyte precursor cells (OPCs) contact sprouting endothelial tip cells in mouse, ferret and human neonatal white matter. Using transgenic mice, we show that increased or decreased OPC density results in cognate changes in white matter vascular investment. Hypoxia promoted both increased OPC numbers and higher white matter vessel density, and endothelial cell expression of the Wnt pathway targets Apcdd1 and Axin2, suggesting paracrine OPC-endothelial signaling. Conditional knockout of OPC Wntless resulted in diminished w…

0301 basic medicineGenetically modified mouseoligodendrocytesMice TransgenicBiologyArticleWhite matter03 medical and health sciencesParacrine signallingMice0302 clinical medicinetip cell angiogenesisAxin ProteinConditional gene knockoutmedicineAXIN2AnimalsHumanshypoxic-ischemic encephalopathyHypoxiaWnt Signaling PathwayGeneral NeuroscienceWnt signaling pathwayFerretsIntracellular Signaling Peptides and ProteinsEndothelial CellsMembrane ProteinsCell DifferentiationHypoxia (medical)Wnt signalingWhite Matter3. Good healthCell biologyEndothelial stem cellstomatognathic diseasesOligodendroglia030104 developmental biologymedicine.anatomical_structurenervous systemEndothelium Vascularmedicine.symptom030217 neurology & neurosurgeryNeuron
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TMIC-49. POTASSIUM CHANNEL KIR4.1 AND GLUTAMINE SYNTHETASE ARE DYSREGULATED IN GLIOMA

2017

The potassium channel KIR4.1 (KCNJ10) and the glutamate catalyzing enzyme glutamine synthetase (GS) are highly expressed in glial cells of the central nervous system. Both glial proteins play important roles in the maintenance of neuronal activity and neurotransmission. Dysfunction of both proteins can result in altered neuronal excitability and may lead to excitotoxicity. We analyzed 35 snap frozen tissue blocks (glioblastoma [GBM], n=22; low grade astrocytoma (LGA), n=8; oligodendroglioma (OG), n=3; oligoastrocytoma, n=2). All glioma samples had a matching tissue specimen from both the tumor core and the adjacent normal-appearing infiltration zone. Molecular subtyping (MGMT, IDH1/2, 1p/19…

Cancer ResearchChemistryGlutamate receptorExcitotoxicitymedicine.diseasemedicine.disease_causePotassium channelAbstractsmedicine.anatomical_structureOncologyGlutamine synthetaseGliomaGene expressionCancer researchmedicineNeurogliaNeurology (clinical)Oligodendroglioma
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