Search results for " Neuronal"

showing 10 items of 222 documents

Altered morphological and electrophysiological properties of Cajal-Retzius cells in cerebral cortex of embryonic Presenilin-1 knockout mice

2004

Mutations of Presenilin-1 are the major cause of familial Alzheimer's disease. Presenilin-1 knockout (PS1-/-) mice develop severe cortical dysplasia related to human type 2 lissencephaly. This overmigration syndrome has been attributed to the premature loss of Cajal-Retzius cells (CRcs), pioneer neurons required for the termination of radial neuronal migration. To elucidate the potential cellular mechanisms responsible for this premature neuronal loss, we investigated the morphological and electrophysiological properties of visually identified CRcs of wild-type (WT) and PS1-/- mouse brains at embryonic day 16.5. The density of CRcs was substantially reduced in the cerebral cortex of PS1-/-.…

Cell Adhesion Molecules NeuronalNerve Tissue ProteinsBiologyBicucullineMembrane PotentialsGABA AntagonistsMicemental disordersExcitatory Amino Acid AgonistsPresenilin-1medicineAnimalsneoplasms6-Cyano-7-nitroquinoxaline-23-dioneCerebral CortexMice KnockoutNeuronsMembrane potentialExtracellular Matrix ProteinsGABAA receptorStem CellsGeneral NeuroscienceSerine EndopeptidasesExcitatory Postsynaptic PotentialsMembrane ProteinsCortical dysplasiaBicucullineEmbryo Mammalianmedicine.diseaseImmunohistochemistryElectric Stimulationdigestive system diseasesnervous system diseasesCell biologyReelin ProteinElectrophysiologymedicine.anatomical_structure2-Amino-5-phosphonovaleratenervous systemCerebral cortexKnockout mouseExcitatory postsynaptic potentialExcitatory Amino Acid AntagonistsNeurosciencemedicine.drugEuropean Journal of Neuroscience
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Expression of M-cadherin protein in myogenic cells during prenatal mouse development and differentiation of embryonic stem cells in culture.

1994

Molecules regulating morphogenesis by cell-cell interactions are the cadherins, a class of calcium-dependent adhesion molecules. One of its members, M-cadherin, has been isolated from a myoblast cell line (Donalies et al. [1991] Proc. Natl. Acad. Sci. U.S.A. 88:8024—8028). In mouse development, expression of M-cadherin mRNA first appears at day 8.5 of gestation (E8.5) in somites and has been postulated to be down-regulated in developing muscle masses (Moore and Walsh [1993] Development 117:1409—1420). Affinity-purified polyclonal M-cadherin antibodies, detecting a protein of approximately 120 kDa, were used to study the cell expression pattern of M-cadherin protein. It was first visualized …

Cell Adhesion Molecules NeuronalRecombinant Fusion ProteinsMolecular Sequence DataMorphogenesisFluorescent Antibody TechniqueGestational AgeBiologyEmbryonic and Fetal DevelopmentMiceLamininPregnancyMyocyteAnimalsAmino Acid SequenceRNA MessengerMuscle SkeletalCells CulturedDNA PrimersMice Inbred BALB CBase SequenceCadherinCell adhesion moleculeStem CellsCell MembraneGene Expression Regulation DevelopmentalCadherinsEmbryonic stem cellMolecular biologyCell culturebiology.proteinDesminFemaleDevelopmental BiologyDevelopmental dynamics : an official publication of the American Association of Anatomists
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The MDM2-p53 pathway is involved in preconditioning-induced neuronal tolerance to ischemia

2018

Brain preconditioning (PC) refers to a state of transient tolerance against a lethal insult that can be evoked by a prior mild event. It is thought that PC may induce different pathways responsible for neuroprotection, which may involve the attenuation of cell damage pathways, including the apoptotic cell death. In this context, p53 is a stress sensor that accumulates during brain ischemia leading to neuronal death. The murine double minute 2 gene (MDM2), a p53-specific E3 ubiquitin ligase, is the main cellular antagonist of p53, mediating its degradation by the proteasome. Here, we study the role of MDM2-p53 pathway on PC-induced neuroprotection both in cultured neurons (in vitro) and rat …

Cell death0301 basic medicineProgrammed cell deathCell SurvivalNeuronalScience2415 Biología MolecularIschemiaNeuroprotectionArticleBrain ischemiaMiceBrain ischemia03 medical and health sciences0302 clinical medicineIschemiaXarxes neuronals (Neurobiologia)medicineAnimalsIschemic PreconditioningCell damageCells CulturedBrain preconditioningNeuronsMultidisciplinarybiologyChemistryQRBrainProto-Oncogene Proteins c-mdm2MDM2-p53medicine.diseaseNeuroprotectionRatsCell biologyUbiquitin ligaseDisease Models Animal030104 developmental biology2490 Neurocienciasbiology.proteinMedicineIschemic preconditioningMdm2Tumor Suppressor Protein p53030217 neurology & neurosurgerySignal Transduction
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Alternative splicing products of the tenascin gene distinguish rat liver fat storing cells from arterial smooth muscle cells and skin fibroblasts

1992

Abstract Fat storing-(Ito-)cells (FSC) transform into a myofibroblast-like cell type during liver fibrogenesis. A similar development can be observed in cell culture. At the moment, a definite marker to differentiate transformed FSC from smooth muscle cells (SMC) is not available. We recently found that FSC, SMC and skin fibroblasts (SF) synthesize tenascin, a novel matrix protein. As it is reported that various tissues express different tenascin forms by the mechanism of alternative pre-mRNA splicing, we analyzed the tenascin transcripts in these cell types. Total RNA extracted from cultured FSC, SMC and SF, analyzed by Northern blot hybridization, showed a 7.2 kb transcript in FSC, a 8.7 …

Cell typeCell Adhesion Molecules NeuronalRNA SplicingMolecular Sequence DataBiophysicsGene ExpressionTenascinBiochemistryExtracellular matrixTransforming Growth Factor betaGene expressionAnimalsRNA MessengerNorthern blotMolecular BiologyExtracellular Matrix ProteinsMessenger RNABase SequencebiologyAlternative splicingCell DifferentiationMuscle SmoothRats Inbred StrainsTenascinCell BiologyFibroblastsmusculoskeletal systemMolecular biologyFibronectinsRatsCytoskeletal ProteinsAdipose TissueOligodeoxyribonucleotidesRNA splicingbiology.proteinBiochemical and Biophysical Research Communications
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Immunoproteomic studies on paediatric opsoclonus-myoclonus associated with neuroblastoma

2016

We aimed to identify new cell-membrane antigens implicated in opsoclonus-myoclonus with neuroblastoma. The sera of 3 out of 14 patients showed IgG electron-microscopy immunogold reactivity on SH-SY5Y neuroblastoma cells. Immunoprecipitation experiments using rat brain synaptosomes and SH-SY5Y cells led to the identification of: (1) thirty-one nuclear/cytoplasmic proteins (including antigens HuB, HuC); (2) seven neuronal membrane proteins, including the Shaw-potassium channel Kv3.3 (KCNC3), whose genetic disruption in mice causes ataxia and generalized muscle twitching. Although cell-based assays did not demonstrate direct antigenicity, our findings point to Shaw-related subfamily of the pot…

Central Nervous SystemMale0301 basic medicineAntigenicityDatabases FactualThymomaImmunoprecipitationKCTD7Cell Adhesion Molecules NeuronalImmunologyNerve Tissue ProteinsBiologyNeuroblastoma03 medical and health sciences0302 clinical medicineAntigenCell Line TumorNeuroblastomaOpsoclonus myoclonus syndromemedicineAnimalsHumansImmunology and AllergyRats WistarChildOpsoclonus-Myoclonus SyndromeBrain NeoplasmsMembrane ProteinsNuclear ProteinsImmunogold labellingmedicine.diseaseMolecular biologyRatsHEK293 Cells030104 developmental biologyShaw Potassium ChannelsNeurologyMembrane proteinEncephalitisFemaleNeurology (clinical)030217 neurology & neurosurgerySynaptosomesJournal of Neuroimmunology
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Central Modulatory Neurons Control Fuel Selection in Flight Muscle of Migratory Locust

2003

Insect flight is one of the most intense and energy-demanding physiological activities. High carbohydrate oxidation rates are necessary for take-off, but, to spare the limited carbohydrate reserves, long-distance flyers, such as locusts, soon switch to lipid as the main fuel. We demonstrate that before a flight, locust muscles are metabolically poised for take-off by the release of octopamine from central modulatory dorsal unpaired median (DUM) neurons, which increases the levels of the potent glycolytic activator fructose 2,6-bisphosphate in flight muscle. Because DUM neurons innervating the flight muscles are active during rest but selectively inhibited during flight, they stimulate carbo…

Central Nervous SystemMalemedicine.medical_specialtyGrasshoppersBrief CommunicationInsect flightCarbohydrate catabolismInternal medicinemedicineFructosediphosphatesPremovement neuronal activityAnimalsGlycolysisProtein kinase AMuscle SkeletalOctopamineNeuronsbiologyGeneral NeuroscienceMigratory locustbiology.organism_classificationCyclic AMP-Dependent Protein KinasesEndocrinologyFlight AnimalOctopamine (neurotransmitter)FemaleGlycolysisLocustSignal Transduction
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Neuronal Activity Drives Localized Blood-Brain-Barrier Transport of Serum Insulin-like Growth Factor-I into the CNS

2010

Upon entry into the central nervous system (CNS), serum insulin-like growth factor-1 (IGF-I) modulates neuronal growth, survival, and excitability. Yet mechanisms that trigger IGF-I entry across the blood-brain barrier remain unclear. We show that neuronal activity elicited by electrical, sensory, or behavioral stimulation increases IGF-I input in activated regions. Entrance of serum IGF-I is triggered by diffusible messengers (i.e., ATP, arachidonic acid derivatives) released during neurovascular coupling. These messengers stimulate matrix metalloproteinase-9, leading to cleavage of the IGF binding protein-3 (IGFBP-3). Cleavage of IGFBP-3 allows the passage of serum IGF-I into the CNS thro…

Central Nervous SystemTime FactorsMicrodialysismedicine.medical_treatmentAction PotentialsStimulationFunctional LateralityBody TemperatureReceptor IGF Type 1chemistry.chemical_compoundNeural PathwaysPremovement neuronal activityDrug InteractionsInsulin-Like Growth Factor IMicroscopy ImmunoelectronReceptorCells CulturedNeuronsGeneral NeuroscienceSysneuro//purl.org/becyt/ford/3.1 [https]Protein TransportMedicina Básicamedicine.anatomical_structureMatrix Metalloproteinase 9Blood-Brain BarrierSIGNALING//purl.org/becyt/ford/3 [https]Arachidonic acidNeurogliaLow Density Lipoprotein Receptor-Related Protein-1CIENCIAS MÉDICAS Y DE LA SALUDNeuroscience(all)Central nervous systemNeurocienciasBiophysicsGlutamic AcidEnzyme-Linked Immunosorbent AssayNerve Tissue ProteinsBiologyBlood–brain barrierMOLNEUROmedicineAnimalsHumansImmunoprecipitationRats WistarAnalysis of VarianceGrowth factorEndothelial CellsTransporterCoculture TechniquesElectric StimulationSignalingRatsMolneurochemistryRegional Blood FlowVibrissaeSYSNEURODigoxigeninExcitatory Amino Acid AntagonistsNeuroscience
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Efectos de la exposición crónica al etanol sobre el tráfico intracelular y citoesqueleto como factores implicados en la migración neuronal

2013

El consumo de etanol durante la gestación puede inducir una serie de alteraciones graves en el desarrollo del feto, la manifestación más extrema da lugar al Síndrome Alcohólico Fetal (SAF). La exposición prenatal al alcohol es la causa conocida y, además evitable, más importante de retraso mental en el mundo occidental. Además de déficits cognitivos, los niños con SAF presentan múltiples anomalías estructurales en el sistema nervioso central, como reducción de la masa cerebral, y a nivel celular, daños en la migración neuronal, en el proceso de formación de espinas dendríticas y establecimiento de sinapsis. En la actualidad, los mecanismos moleculares implicados en la teratogénesis inducida…

Central Nervous Systemaparato de Golgietanolespinas dendríticasneuronasneurons:CIENCIAS DE LA VIDA::Neurociencias [UNESCO]migración neuronalMAP2Fetal Alcoholic SyndromeRho GTPasasactinaRho GTPasesendocitosis:CIENCIAS MÉDICAS::Toxicología [UNESCO]endocytosismicrotúbuloneuronal migrationUNESCO::CIENCIAS MÉDICAS::Toxicologíatráfico intracelularUNESCO::CIENCIAS DE LA VIDA::Biología celular::Cultivo celularcytoskeletondendritic spinesSAFSíndrome Alcohólico Fetalcitoesqueleto:CIENCIAS DE LA VIDA::Biología celular::Cultivo celular [UNESCO]Golgi apparatusUNESCO::CIENCIAS DE LA VIDA::Neurocienciasethanolintracellular trafficactinSistema Nervioso Centralmicrotubule
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Lissencephalic syndromes: brain and beyond

2009

Lissencephaly has been long maintained a malformation involving only the brain. Classic lissencephaly includes agyria and pachygyria and it is the most severe form of malformations derived from abnormal neuronal migration. It is defined as a smooth or nearly smooth cerebral surface with absence of normal sulci and gyria. It encompasses a group of syndromes which show many different clinical conditions. Four groups are actually distinguished: classic lissencephaly variants, other lissencephalies including forms with unknown pathogenesis, microlissencephaly spectrum and Cobblestone cortical malformations. Several genes and proteins are involved in this syndromic spectrum and each year new mol…

Cerebral CortexNeuronsClassical LissencephalyGeneral Immunology and MicrobiologyPachygyriaCortical malformationsLissencephalyBrainCell movementSyndromeBiologymedicine.diseaseGeneral Biochemistry Genetics and Molecular BiologyMicrolissencephalySettore MED/38 - Pediatria Generale E SpecialisticaLissencephaliesCell Movementlissencephaly wide heterogeneitymedicineHumansLissencephalyNeuroscienceAbnormal neuronal migration
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Activity-Dependent Regulation of Neuronal Apoptosis in Neonatal Mouse Cerebral Cortex

2007

A massive neuronal loss during early postnatal development has been well documented in the murine cerebral cortex, but the factors that drive cells into apoptosis are largely unknown. The role of neuronal activity in developmental apoptosis was studied in organotypic neocortical slice cultures of newborn mice. Multielectrode array and whole-cell patch-clamp recordings revealed spontaneous network activity characterized by synchronized burst discharges, which could be blocked by tetrodotoxin and ionotropic glutamate receptor antagonists. The identical neuropharmacological manipulations also caused a significant increase in the number of apoptotic neurons as early as 6 h after the start of dr…

Cerebral CortexNeuronsMice Inbred BALB CNeocortexCognitive NeuroscienceGlutamate receptorAction PotentialsApoptosisBiologyReceptors N-Methyl-D-AspartateNeuroprotectionMiceCellular and Molecular NeuroscienceOrgan Culture Techniquesmedicine.anatomical_structureAnimals NewbornCerebral cortexTrk receptormedicineAnimalsNMDA receptorPremovement neuronal activityNeuroscienceIonotropic effectCerebral Cortex
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