2014
Ablation of ErbB4 from excitatory neurons leads to reduced dendritic spine density in mouse prefrontal cortex
Cooper MA, Koleske AJ. Ablation of ErbB4 from excitatory neurons leads to reduced dendritic spine density in mouse prefrontal cortex. The Journal Of Comparative Neurology 2014, 522: 3351-3362. PMID: 24752666, PMCID: PMC4107058, DOI: 10.1002/cne.23615.Peer-Reviewed Original ResearchMeSH KeywordsAge FactorsAnimalsCalcium-Calmodulin-Dependent Protein Kinase Type 2Cell FractionationCells, CulturedDendritic SpinesDisks Large Homolog 4 ProteinGene Expression RegulationGreen Fluorescent ProteinsGuanylate KinasesMembrane ProteinsMiceMice, TransgenicMitogen-Activated Protein Kinase 3NestinNeuronsPrefrontal CortexReceptor, ErbB-4SynapsesTransfectionConceptsDendritic spine densitySpine densityExcitatory pyramidal cellsExcitatory neuronsPrefrontal cortexPyramidal cellsDendritic spinesErbB4 functionAblation of ErbB4Dendritic spine lossCortical neuronal culturesMouse prefrontal cortexDendritic spine developmentMonths of ageSynaptic plasma membrane preparationsSpine lossWeanling miceDorsomedial prefrontal cortexPsychiatric disordersKnockout miceMature spinesErbB4 signalingSynaptic plasticityNeuronal culturesDisease pathology
2013
Delayed amyloid plaque deposition and behavioral deficits in outcrossed AβPP/PS1 mice
Couch BA, Kerrisk ME, Kaufman AC, Nygaard HB, Strittmatter SM, Koleske AJ. Delayed amyloid plaque deposition and behavioral deficits in outcrossed AβPP/PS1 mice. The Journal Of Comparative Neurology 2013, 521: 1395-1408. PMID: 23047754, PMCID: PMC3562562, DOI: 10.1002/cne.23239.Peer-Reviewed Original ResearchConceptsAβPP/PS1 micePS1 micePlaque burdenPlaque depositionBehavioral deficitsRadial arm water maze performanceBehavioral impairmentsAlzheimer's diseaseAβPP processingPresenilin 1Amyloid-β precursor proteinLower plaque burdenProgressive neurodegenerative dementiaAmyloid plaque depositionAmyloid plaque accumulationAmyloid plaque burdenAD-like featuresNovel object recognitionWater maze performanceMonths of ageDendrite lossAD progressionNeurodegenerative dementiaPlaque accumulationMixed genetic background