Search results for "Transgenic"

showing 10 items of 552 documents

Primary cilia are required for cerebellar development and Shh-dependent expansion of progenitor pool

2008

Cerebellar granule cell precursors (GCPs), which give rise to the most abundant neuronal type in the mammalian brain, arise from a restricted pool of primary progenitors in the rhombic lip (RL). Sonic hedgehog (Shh) secreted by developing Purkinje cells is essential for the expansion of GCPs and for cerebellar morphogenesis. Recent studies have shown that the primary cilium concentrates components of Shh signaling and that this structure is required for Shh signaling. GCPs have a primary cilium on their surface [Del Cerro, M.P., Snider, R.S. (1972). Studies on the developing cerebellum. II. The ultrastructure of the external granular layer. J Comp Neurol 144, 131-64.]. Here, we show that 1)…

CerebellumKinesinsReceptors G-Protein-CoupledMicePurkinje Cells0302 clinical medicinePrimary ciliaCerebellumSonic hedgehogPromoter Regions GeneticRhombic lipGenetics0303 health scienceseducation.field_of_studyCiliumStem CellsSonic hedgehogjoubert syndromeCerebellar developmentSmoothened ReceptorCell biologyneurogenesismedicine.anatomical_structurecerebellar developmentembryonic structuresanimal structuresNeurogenesisPopulationMice TransgenicBiologyKif3aArticle03 medical and health sciencessonic hedgehogprimary ciliaJoubert syndromeGlial Fibrillary Acidic ProteinmedicineAnimalsHumansKIF3AHedgehog ProteinsCiliaeducationMolecular Biology030304 developmental biologyCell BiologyGranule cellMice Inbred C57BLbiology.proteinSmoothened030217 neurology & neurosurgeryDevelopmental Biology
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Purkinje cell loss and motor coordination defects in profilin1 mutant mice.

2012

Profilin1 is an actin monomer-binding protein, essential for cytoskeletal dynamics. Based on its broad expression in the brain and the localization at excitatory synapses (hippocampal CA3-CA1 synapse, cerebellar parallel fiber (PF)-Purkinje cell (PC) synapse), an important role for profilin1 in brain development and synapse physiology has been postulated. We recently showed normal physiology of hippocampal CA3-CA1 synapses in the absence of profilin1, but impaired glial cell binding and radial migration of cerebellar granule neurons (CGNs). Consequently, brain-specific inactivation of profilin1 by exploiting conditional mutants and Nestin-mediated cre expression resulted in a cerebellar hyp…

CerebellumPatch-Clamp TechniquesPurkinje cellBiophysicsAction PotentialsParallel fiberMice TransgenicNerve Tissue ProteinsBiologyHippocampal formationIn Vitro TechniquesMotor ActivitySynapseNestinMiceProfilinsPurkinje CellsIntermediate Filament ProteinsmedicineAnimalsGeneral NeuroscienceAge FactorsBrainGene Expression Regulation DevelopmentalLong-term potentiationElectric StimulationDisease Models Animalmedicine.anatomical_structurenervous systemCytoarchitectureAnimals NewbornCerebellar cortexMutationDisease ProgressionPsychomotor DisordersNeuroscienceNeuroscience
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The angiopoietin-Tie2 pathway regulates Purkinje cell dendritic morphogenesis in a cell-autonomous manner.

2021

Neuro-vascular communication is essential to synchronize central nervous system development. Here, we identify angiopoietin/Tie2 as a neuro-vascular signaling axis involved in regulating dendritic morphogenesis of Purkinje cells (PCs). We show that in the developing cerebellum Tie2 expression is not restricted to blood vessels, but it is also present in PCs. Its ligands angiopoietin-1 (Ang1) and angiopoietin-2 (Ang2) are expressed in neural cells and endothelial cells (ECs), respectively. PC-specific deletion of Tie2 results in reduced dendritic arborization, which is recapitulated in neural-specific Ang1-knockout and Ang2 full-knockout mice. Mechanistically, RNA sequencing reveals that Tie…

CerebellumalphaCytoskeleton organizationAngiogenesisPurkinje cellprotocadherinsMorphogenesisneural progenitor cellsMice Transgenicself-avoidanceBiologyModels BiologicalGeneral Biochemistry Genetics and Molecular BiologyAngiopoietinAngiopoietin-2Purkinje Cellsddc:570CerebellumexpressionGene expressionmedicineAngiopoietin-1MorphogenesisAnimalsmouseMice KnockoutIntegrasessubventricular zonedifferentiationDendritesmtorc2Angiopoietin receptorReceptor TIE-2Cell biologyMice Inbred C57BLmedicine.anatomical_structuremessenger-rnaGene Expression RegulationOrgan Specificityembryonic structurescardiovascular systembiology.proteinGene DeletionSignal TransductionCell reports
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Making Waves: Initiation and Propagation of Corticothalamic Ca2+ Waves In Vivo

2013

Corticothalamic slow oscillations of neuronal activity determine internal brain states. At least in the cortex, the electrical activity is associated with large neuronal Ca(2+) transients. Here we implemented an optogenetic approach to explore causal features of the generation of slow oscillation-associated Ca(2+) waves in the in vivo mouse brain. We demonstrate that brief optogenetic stimulation (3-20 ms) of a local group of layer 5 cortical neurons is sufficient for the induction of global brain Ca(2+) waves. These Ca(2+) waves are evoked in an all-or-none manner, exhibit refractoriness during repetitive stimulation, and propagate over long distances. By local optogenetic stimulation, we …

Cerebral CortexRefractory periodGeneral NeuroscienceNeuroscience(all)ThalamusMice TransgenicStimulationCortical neuronsBiologyOptogeneticsCortex (botany)Mice Inbred C57BLOptogeneticsMiceThalamusIn vivoNeural PathwaysAnimalsPremovement neuronal activityCalcium SignalingNeurosciencePhotic StimulationVisual CortexNeuron
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Dual effects of increased glycogen synthase kinase-3β activity on adult neurogenesis

2013

Adult neurogenesis, the generation of new neurons during the adulthood, is a process controlled by several kinases and phosphatases among which GSK3β exerts important functions. This protein is particularly abundant in the central nervous system, and its activity deregulation is believed to play a key role in chronic disorders such as Alzheimer's disease. Previously, we reported that in vivo overexpression of GSK3β (Tet/GSK3β mice) causes alterations in adult neurogenesis, leading to a depletion of the neurogenic niches. Here, we have further characterized those alterations, finding a delay in the switching-off of doublecortin marker as well as changes in the survival and death rates of imm…

Chemokine CCL11Doublecortin Domain ProteinsCell SurvivalNeurogenesisTransgeneCentral nervous systemMice TransgenicNerve Tissue ProteinsBiologySubgranular zoneNestinGlycogen Synthase Kinase 3MiceIntermediate Filament ProteinsNeural Stem CellsGenes ReporterGlial Fibrillary Acidic ProteinGeneticsmedicineAnimalsStem Cell NicheMolecular BiologyGSK3BGenetics (clinical)NeuronsGlycogen Synthase Kinase 3 betaNeuropeptidesNeurogenesisNuclear ProteinsGeneral MedicineNestinbeta-GalactosidaseCell biologyDoublecortinDNA-Binding ProteinsMice Inbred C57BLmedicine.anatomical_structureEnzyme InductionDentate GyrusImmunologybiology.proteinMicrotubule-Associated ProteinsNeural developmentBiomarkersHuman Molecular Genetics
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IL-23-mediated mononuclear phagocyte crosstalk protects mice from Citrobacter rodentium-induced colon immunopathology.

2014

Gut homeostasis and mucosal immune defense rely on the differential contributions of dendritic cells (DC) and macrophages. Here we show that colonic CX3CR1+ mononuclear phagocytes are critical inducers of the innate response to Citrobacter rodentium infection. Specifically, the absence of IL-23 expression in macrophages or CD11b+ DC results in the impairment of IL-22 production and in acute lethality. Highlighting immunopathology as a death cause, infected animals are rescued by the neutralization of IL-12 or IFNγ. Moreover, mice are also protected when the CD103+ CD11b− DC compartment is rendered deficient for IL-12 production. We show that IL-12 production by colonic CD103+ CD11b− DC is r…

ChemokineColonCX3C Chemokine Receptor 1General Physics and Astronomychemical and pharmacologic phenomenaMice TransgenicInterleukin-23General Biochemistry Genetics and Molecular BiologyMonocytesArticleMicrobiologyInterferon-gammaMiceIntestinal mucosaAntigens CDImmunopathologyCitrobacter rodentiummedicineAnimalsHomeostasisInterferon gammaIntestinal MucosaImmunity MucosalMultidisciplinaryCD11b AntigenbiologyInterleukinsMacrophagesEnterobacteriaceae InfectionsGeneral ChemistryMononuclear phagocyte systemDendritic CellsInterleukin-12Survival AnalysisImmunity InnateIntegrin alpha MGene Expression RegulationImmunologyInterleukin 12biology.proteinCitrobacter rodentiumTh17 CellsReceptors ChemokineIntegrin alpha Chainsmedicine.drugSignal TransductionNature communications
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Influenza A virus infection inhibits the efficient recruitment of Th2 cells into the airways and the development of airway eosinophilia.

2003

Abstract Most infections with respiratory viruses induce Th1 responses characterized by the generation of Th1 and CD8+ T cells secreting IFN-γ, which in turn have been shown to inhibit the development of Th2 cells. Therefore, it could be expected that respiratory viral infections mediate protection against asthma. However, the opposite seems to be true, because viral infections are often associated with the exacerbation of asthma. For this reason, we investigated what effect an influenza A (flu) virus infection has on the development of asthma. We found that flu infection 1, 3, 6, or 9 wk before allergen airway challenge resulted in a strong suppression of allergen-induced airway eosinophil…

ChemokineEpitopes T-LymphocyteImmunoglobulin Emedicine.disease_causeMiceCell MovementInfluenza A virusImmunology and AllergyEosinophiliaChemokine CCL5LungCells CulturedChemokine CCL2Mice KnockoutMice Inbred BALB Cbiologymedicine.diagnostic_testrespiratory systemUp-Regulationmedicine.anatomical_structureInfluenza A virusChemokines CCGoblet CellsNippostrongylusmedicine.symptomBronchial HyperreactivityChemokine CCL11OvalbuminImmunologyDown-RegulationMice TransgenicCCL5VirusInterferon-gammaTh2 CellsOrthomyxoviridae InfectionsLymphopeniamedicineAnimalsLymphocyte CountPulmonary EosinophiliaStrongylida InfectionsGoblet cellMetaplasiaAllergensPeptide Fragmentsrespiratory tract diseasesMice Inbred C57BLBronchoalveolar lavageImmunologyCell Migration Inhibitionbiology.proteinInterleukin-5Journal of immunology (Baltimore, Md. : 1950)
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Role of the chemokine decoy receptor D6 in balancing inflammation, immune activation, and antimicrobial resistance in Mycobacterium tuberculosis infe…

2008

D6 is a decoy and scavenger receptor for inflammatory CC chemokines. D6-deficient mice were rapidly killed by intranasal administration of low doses of Mycobacterium tuberculosis. The death of D6(-/-) mice was associated with a dramatic local and systemic inflammatory response with levels of M. tuberculosis colony-forming units similar to control D6-proficient mice. D6-deficient mice showed an increased numbers of mononuclear cells (macrophages, dendritic cells, and CD4 and CD8 T lymphocytes) infiltrating inflamed tissues and lymph nodes, as well as abnormal increased concentrations of CC chemokines (CCL2, CCL3, CCL4, and CCL5) and proinflammatory cytokines (tumor necrosis factor alpha, int…

Chemokinedecoy receptor inflammation Mycobacterium tuberculosis infectionmedicine.medical_treatmentInterleukin-1betaImmunologyMice TransgenicInflammationReceptors CCR10BiologyModels BiologicalArticleCCL5Proinflammatory cytokineInterferon-gammaMiceImmune systemAnti-Infective AgentsDrug Resistance BacterialmedicineAnimalsImmunology and AllergyInterferon gammaInflammationTumor Necrosis Factor-alphaArticlesMycobacterium tuberculosisPhenotypeCytokineImmune SystemImmunologybiology.proteinTumor necrosis factor alphaLymph Nodesmedicine.symptommedicine.drug
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Satb2 Regulates Callosal Projection Neuron Identity in the Developing Cerebral Cortex

2008

SummarySatb2 is a DNA-binding protein that regulates chromatin organization and gene expression. In the developing brain, Satb2 is expressed in cortical neurons that extend axons across the corpus callosum. To assess the role of Satb2 in neurons, we analyzed mice in which the Satb2 locus was disrupted by insertion of a LacZ gene. In mutant mice, β-galactosidase-labeled axons are absent from the corpus callosum and instead descend along the corticospinal tract. Satb2 mutant neurons acquire expression of Ctip2, a transcription factor that is necessary and sufficient for the extension of subcortical projections by cortical neurons. Conversely, ectopic expression of Satb2 in neural stem cells m…

Chromatin ImmunoprecipitationNeuroscience(all)Electrophoretic Mobility Shift AssayMice TransgenicNerve Tissue ProteinsDEVBIOBiologyCorpus callosumMOLNEUROMiceNeural PathwaysmedicineAnimalsCells CulturedCerebral CortexNeuronsRegulation of gene expressionStem CellsGeneral NeuroscienceGene Expression Regulation DevelopmentalMatrix Attachment Region Binding ProteinsDNAEmbryo MammalianNeural stem cellChromatinmedicine.anatomical_structureAnimals NewbornBromodeoxyuridinenervous systemCerebral cortexRegulatory sequenceMutationCorticospinal tractEctopic expressionNeuroscienceTranscription Factors
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Haploinsufficiency of Tsc2 Leads to Hyperexcitability of Medial Prefrontal Cortex via Weakening of Tonic GABAB Receptor-mediated Inhibition.

2020

Abstract Loss-of-function mutation in one of the tumor suppressor genes TSC1 or TSC2 is associated with several neurological and psychiatric diseases, including autism spectrum disorders (ASDs). As an imbalance between excitatory and inhibitory neurotransmission, E/I ratio is believed to contribute to the development of these disorders, we investigated synaptic transmission during the first postnatal month using the Tsc2+/− mouse model. Electrophysiological recordings were performed in acute brain slices of medial prefrontal cortex. E/I ratio at postnatal day (P) 15–19 is increased in Tsc2+/− mice as compared with wildtype (WT). At P25–30, facilitated GABAergic transmission reduces E/I rati…

Cognitive NeurosciencePrefrontal CortexMice TransgenicHaploinsufficiencyGABAB receptorNeurotransmissionInhibitory postsynaptic potentialSynaptic TransmissionTonic (physiology)03 medical and health sciencesCellular and Molecular Neurosciencechemistry.chemical_compound0302 clinical medicineTuberous Sclerosis Complex 2 ProteinAnimalsPrefrontal cortex030304 developmental biologyNeurons0303 health sciencesChemistryElectrophysiologyBaclofenReceptors GABA-BExcitatory postsynaptic potentialNeuroscience030217 neurology & neurosurgeryCerebral cortex (New York, N.Y. : 1991)
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