2012
NKCC1 Knockdown Decreases Neuron Production through GABAA-Regulated Neural Progenitor Proliferation and Delays Dendrite Development
Young SZ, Taylor MM, Wu S, Ikeda-Matsuo Y, Kubera C, Bordey A. NKCC1 Knockdown Decreases Neuron Production through GABAA-Regulated Neural Progenitor Proliferation and Delays Dendrite Development. Journal Of Neuroscience 2012, 32: 13630-13638. PMID: 23015452, PMCID: PMC3478384, DOI: 10.1523/jneurosci.2864-12.2012.Peer-Reviewed Original ResearchMeSH KeywordsAge FactorsAnalysis of VarianceAnimalsAnimals, NewbornCalciumCell CountCell DifferentiationCell ProliferationCells, CulturedCerebral VentriclesDendritesEgtazic AcidElectroporationFemaleGABA ModulatorsGABA-A Receptor AgonistsGreen Fluorescent ProteinsIn Vitro TechniquesKi-67 AntigenLuminescent ProteinsMaleMiceMuscimolNeural Stem CellsNeuronsOlfactory BulbPatch-Clamp TechniquesPentobarbitalReceptors, GABA-ARNA, Small InterferingSodium-Potassium-Chloride SymportersSolute Carrier Family 12, Member 2SOXB1 Transcription FactorsTransfectionConceptsNPC proliferationDecreased neuronal densityTotal dendritic lengthNeonatal subventricular zoneNeural stem cell proliferationNeural progenitor cell developmentNeural progenitor proliferationShort hairpin RNADendritic complexityDendritic lengthNeuronal densityNewborn neuronsDendritic arborizationNeuron densityDendritic developmentSubventricular zoneNeuron productionCalcium responseSynaptic integrationNKCC1 knockdownPentobarbital effectsAllosteric agonistDendritic treeProgenitor cell developmentCotransporter NKCC1
2005
Nonsynaptic GABA signaling in postnatal subventricular zone controls proliferation of GFAP-expressing progenitors
Liu X, Wang Q, Haydar TF, Bordey A. Nonsynaptic GABA signaling in postnatal subventricular zone controls proliferation of GFAP-expressing progenitors. Nature Neuroscience 2005, 8: 1179-1187. PMID: 16116450, PMCID: PMC1380263, DOI: 10.1038/nn1522.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnimals, NewbornBotulinum ToxinsBromodeoxyuridineCadmiumCell CountCell ProliferationChelating AgentsCyclooxygenase InhibitorsDose-Response Relationship, DrugDose-Response Relationship, RadiationDrug InteractionsEgtazic AcidElectric StimulationEnzyme InhibitorsGABA AntagonistsGamma-Aminobutyric AcidGene Expression RegulationGlial Fibrillary Acidic ProteinGreen Fluorescent ProteinsImmunohistochemistryIn Vitro TechniquesLateral VentriclesMeclofenamic AcidMembrane PotentialsMiceMice, TransgenicNeuronsNickelPatch-Clamp TechniquesPotassiumSodium Channel BlockersSpider VenomsStem CellsTetrodotoxinConceptsPostnatal subventricular zoneGFAP-expressing cellsSubventricular zoneCell cycleGABAA receptorsStem cellsNeuroblastsProgenitorsGlial fibrillary acidic proteinSVZ cellsGABAA receptor currentsGABAA receptor activationFibrillary acidic proteinReceptor activationCellsProliferationGABA releaseMouse slicesLocal cuesAcidic proteinReceptor currentsSpontaneous depolarizationsGFAPGABAReceptors
1998
Passive Glial Cells, Fact or Artifact?
Bordey A, Sontheimer H. Passive Glial Cells, Fact or Artifact? The Journal Of Membrane Biology 1998, 166: 213-222. PMID: 9843595, DOI: 10.1007/s002329900463.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsVoltage-activated currentsPassive astrocytesVoltage-dependent outwardCell accessAcute tissue slicesBath Ca2Glial cellsRat hippocampusSlice recordingsCultured astrocytesAstrocytesPipette solutionEffect of Ca2Tissue slicesMembrane capacitanceSuch cellsSubpopulationsCellsTransient maskingConcentration of Ca2Ca2SuperfusionHippocampusDose