Search results for " Neuronal"

showing 10 items of 222 documents

Cellular expression of connexins in the rat brain: neuronal localization, effects of kainate-induced seizures and expression in apoptotic neuronal ce…

2003

The identification of connexins (Cxs) expressed in neuronal cells represents a crucial step for understanding the direct communication between neurons and between neuron and glia. In the present work, using a double-labelling method combining in situ hybridization for Cx mRNAs with immunohistochemical detection for neuronal markers, we provide evidence that, among cerebral connexins (Cx26, Cx32, Cx36, Cx37, Cx40, Cx43, Cx45 and Cx47), only Cx45 and Cx36 mRNAs are localized in neuronal cells in both developing and adult rat brain. In order to establish whether connexin expression is influenced in vivo by abnormal neuronal activity, we examined the short-term effects of kainate-induced seizur…

MaleAgingTime FactorsgliaHippocampusConnexinbrain developmentKainate receptorApoptosisIn situ hybridizationBiologyConnexinsgap junctionbrain development; gap junction; gliaSeizuresTubulinmedicineExcitatory Amino Acid AgonistsIn Situ Nick-End LabelingPremovement neuronal activityAnimalsRNA MessengerOrganic ChemicalsRats WistarIn Situ HybridizationFluorescent DyesNeuronsMessenger RNAKainic AcidReverse Transcriptase Polymerase Chain ReactionGeneral NeuroscienceGap junctionBrainGene Expression Regulation DevelopmentalFluoresceinsImmunohistochemistryCell biologyRatsmedicine.anatomical_structurenervous systemAnimals NewbornPhosphopyruvate HydrataseAutoradiographysense organsNeuronNeuroscienceDensitometryThe European journal of neuroscience
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FGF-2/FGFR1 neurotrophic system expression level and its basal activation do not account for the age-dependent decline of precursor cell proliferatio…

2010

It is largely accepted that neurogenesis in the adult brain decreases with age and reduced levels of local neurotrophic support is speculated to be a contributing factor. Among neurotrophic factors involved on neurogenesis, we focused our attention on the neurotrophic system fibroblast growth factor-2 (FGF-2) and its receptor FGFR1, a potent modulator of precursor cell proliferation. In the present work, we aimed to analyse if potential age-dependent changes of the FGF-2/FGFR1 neurotrophic system may give account for the age-dependent decline of precursor cell proliferation in the neurogenic region of the subventricular zone (SVZ) in the rat brain. Using in situ hybridization and western bl…

MaleAgingmedicine.medical_specialtySubventricular zoneNeurogenesisReceptor expressionFGF-2Subventricular zoneFibroblast growth factorSettore BIO/09 - FisiologiaCerebral VentriclesFGF-2; FGFR1; Neurogenesis; Subventricular zone; Neuronal precursor cells; AgingGrowth factor receptorNeurotrophic factorsInternal medicinePrecursor cellmedicineAnimalsRNA MessengerReceptor Fibroblast Growth Factor Type 1PhosphorylationRats WistarMolecular BiologyCell ProliferationMitogen-Activated Protein Kinase 3biologyPhospholipase C gammaGeneral NeuroscienceNeurogenesisBrainNeuronal precursor cellRatsAdult Stem CellsFGFR1medicine.anatomical_structureEndocrinologyBromodeoxyuridineGene Expression Regulationbiology.proteinFibroblast Growth Factor 1NeurogenesiFibroblast Growth Factor 2Neurology (clinical)Developmental BiologyNeurotrophinBrain Research
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Protective activation of the endocannabinoid system during ischemia in dopamine neurons

2006

Endocannabinoids act as neuroprotective molecules promptly released in response to pathological stimuli. Hence, they may represent one component of protection and/or repair mechanisms mobilized by dopamine (DA) neurons under ischemia. Here, we show that the endocannabinoid 2-arachidonoyl-glycerol (2-AG) plays a key role in protecting DA neurons from ischemia-induced altered spontaneous activity both in vitro and in vivo. Accordingly, neuroprotection can be elicited through moderate cannabinoid receptor type-1 (CB1) activation. Conversely, blockade of endocannabinoid actions through CB1 receptor antagonism worsens the outcome of transient ischemia on DA neuronal activity. These findings indi…

MaleCannabinoid receptorDopaminePharmacologyBrain IschemiaMidbrainRats Sprague-DawleyMicePiperidinesReceptor Cannabinoid CB1IschemiaPremovement neuronal activityReceptorMice KnockoutNeuronsmusculoskeletal neural and ocular physiologyEndocannabinoid systemCB1NeuroprotectionElectrophysiologyNeurologylipids (amino acids peptides and proteins)Rimonabantpsychological phenomena and processesmedicine.drugSignal TransductionMorpholinesIschemiaArachidonic AcidsBiologyIn Vitro TechniquesNaphthalenesNeuroprotectionAmidohydrolasesGlycerideslcsh:RC321-571DopamineCannabinoid Receptor ModulatorsmedicineAnimalslcsh:Neurosciences. Biological psychiatry. NeuropsychiatryEndocannabinoidVentral Tegmental Areamedicine.diseaseBlockadeBenzoxazinesRatsnervous systemPyrazolesNeuroscienceEndocannabinoidsNeurobiology of Disease
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Aberrant arrested in maturation neuromuscular junctions in centronuclear myopathy

1994

Unusual ultrastructural changes of the nerve terminals have been found in an infant born with severe, fatal XLR form of centronuclear myopathy. Aberrant neuromuscular junctions in myotubes decorated by N-CAM were observed. The junction changes were manifested by simplification of postsynaptic membrane and paucity of secondary synaptic clefts. These resembles fetal neuromuscular junctions. The findings suggest that the expression of N-CAM by arrested myotubes may be promoted by abnormal nerve-muscle cell interactions, induced by motor endplate immaturity.

MaleCell Adhesion Molecules NeuronalCellNeuromuscular JunctionElectromyographyBiologyMicrotubulesMotor EndplateNeuromuscular junctionMotor EndplateMicrotubulemedicineHumansCentronuclear myopathyMotor NeuronsFetusTissue Embeddingmedicine.diagnostic_testElectromyographyMyogenesisMusclesInfantNeuromuscular Diseasesmedicine.diseaseCell biologyMicroscopy Electronmedicine.anatomical_structureNeurologySynapsesNeurology (clinical)NeuroscienceJournal of the Neurological Sciences
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Early life stress stimulates hippocampal reelin gene expression in a sex-specific manner: Evidence for corticosterone-mediated action

2010

Early life stress predisposes to the development of psychiatric disorders. In this context the hippocampal formation is of particular interest, because it is affected by stress on the structural and cognitive level. Since little is known how early life stress is translated on the molecular level, we mimicked early life stress in mouse models and analyzed the expression of the glycoprotein Reelin, a master molecule for development and differentiation of the hippocampus. From postnatal day 1 (P1) to P14, mouse pups were subjected to one of the following treatments: nonhandling (NH), handling (H), maternal separation (MS), and early deprivation (ED) followed by immediate (P15) or delayed (P70)…

MaleCell Adhesion Molecules NeuronalCognitive NeuroscienceGene ExpressionCell CountNerve Tissue ProteinsContext (language use)Hippocampal formationHippocampusMiceCajal–Retzius cellchemistry.chemical_compoundSex FactorsCorticosteronemedicineAnimalsRNA MessengerReelinBrain-derived neurotrophic factorExtracellular Matrix ProteinsMaternal deprivationbiologyMaternal DeprivationSerine EndopeptidasesDAB1Reelin Proteinmedicine.anatomical_structurenervous systemchemistrybiology.proteinFemaleCorticosteroneNeuroscienceStress PsychologicalHippocampus
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Glia talk back.

2014

This study shows that the activity of neurons can trigger shedding of a protein, NG2, from the surface of oligodendrocyte precursor cells; this protein in turn modulates synaptic transmission, revealing a two-way conversation between neurons and glia.

MaleCell signalingNeural NetworksQH301-705.5AMPA receptorBiologyNeurotransmissionResearch and Analysis MethodsMechanical Treatment of SpecimensGeneral Biochemistry Genetics and Molecular BiologyBehavioral NeuroscienceNeurotransmitter receptormedicineBiological neural networkPremovement neuronal activityAnimalsBiology (General)AntigensNeuronsGeneral Immunology and MicrobiologyGeneral NeuroscienceMembrane ProteinsBiology and Life SciencesLong-term potentiationADAM ProteinsOligodendrogliamedicine.anatomical_structureElectroporationnervous systemSpecimen DisruptionSpecimen Preparation and TreatmentCellular NeuroscienceImmunologyProteoglycansNeuronAmyloid Precursor Protein SecretasesMolecular NeuroscienceGeneral Agricultural and Biological SciencesNeuroscienceResearch ArticleNeurosciencePLoS biology
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Mutations in the Neuronal Vesicular SNARE VAMP2 Affect Synaptic Membrane Fusion and Impair Human Neurodevelopment

2019

VAMP2 encodes the vesicular SNARE protein VAMP2 (also called synaptobrevin-2). Together with its partners syntaxin-1A and synaptosomal-associated protein 25 (SNAP25), VAMP2 mediates fusion of synaptic vesicles to release neurotransmitters. VAMP2 is essential for vesicular exocytosis and activity-dependent neurotransmitter release. Here, we report five heterozygous de novo mutations in VAMP2 in unrelated individuals presenting with a neurodevelopmental disorder characterized by axial hypotonia (which had been present since birth), intellectual disability, and autistic features. In total, we identified two single-amino-acid deletions and three non-synonymous variants affecting conserved resid…

MaleHeterozygoteAdolescentVesicle-Associated Membrane Protein 2neuronal exocytosisynaptopathyautismsynaptobrevinMembrane FusionExocytosisR-SNARE ProteinsProtein DomainsReportIntellectual DisabilityGeneticsHumansAutistic DisorderChildGenetics (clinical)NeuronsNeurotransmitter Agentsneurodevelopmental disordersvesicle fusionBrainautism; epilepsy; movement disorders; neurodevelopmental disorders; neuronal exocytosis; SNARE; synaptobrevin; synaptopathy; VAMP2; vesicle fusionneuronal exocytosisLipidsMagnetic Resonance Imagingneurodevelopmental disorderautism epilepsy movement disorders neurodevelopmental disorders neuronal exocytosis SNARE synaptobrevin synaptopathy VAMP2 vesicle fusion Genetics Genetics (clinical)Phenotypeautism; epilepsy; movement disorders; neurodevelopmental disorders; neuronal exocytosis; SNARE; synaptobrevin; synaptopathy; VAMP2; vesicle fusion; Genetics; Genetics (clinical)VAMP2SNAREChild PreschoolMutationSynapsesMuscle Hypotoniaepilepsymovement disordersFemalesense organsmovement disorder
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Bruce/apollon promotes hippocampal neuron survival and is downregulated by kainic acid

2005

Prolonged or excess stimulation of excitatory amino acid receptors leads to seizures and the induction of excitotoxic nerve cell injury. Kainic acid acting on glutamate receptors produces degeneration of vulnerable neurons in parts of the hippocampus and amygdala, but the exact mechanisms are not fully understood. We have here investigated whether the anti-apoptotic protein Bruce is involved in kainic acid-induced neurodegeneration. In the rat hippocampus and cortex, Bruce was exclusively expressed by neurons. The levels of Bruce were rapidly downregulated by kainic acid in hippocampal neurons as shown both in vivo and in cell culture. Caspase-3 was activated in neurons exhibiting low level…

MaleKainic acidCell SurvivalBiophysicsExcitotoxicityBruce/apollon Hippocampus Kainic acid Excitotoxicity Neuronal death Caspase-3 Cytochrome cDown-RegulationHippocampusStimulationBiologyHippocampal formationmedicine.disease_causeHippocampusBiochemistrychemistry.chemical_compoundDownregulation and upregulationmedicineAnimalsRats WistarMolecular BiologyCells CulturedNeuronsKainic AcidDose-Response Relationship DrugNeurodegenerationGlutamate receptorCell Biologymedicine.diseaseRatsCell biologynervous systemchemistryBiochemistryUbiquitin-Conjugating Enzymeshuman activitiescirculatory and respiratory physiology
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Zinc chelation during non-lesioning overexcitation results in neuronal death in the mouse hippocampus

2003

In the hippocampus, chelatable zinc is accumulated in vesicles of glutamatergic presynaptic terminals, abounding specially in the mossy fibers, from where it is released with activity and can exert a powerful inhibitory action upon N-methyl-D-aspartate receptors. Zinc is therefore in a strategic situation to control overexcitation at the zinc-rich excitatory synapses, and consequently zinc removal during high activity might result in excitotoxic neuronal damage. We analyzed the effect of zinc chelation with sodium dietyldithiocarbamate under overexcitation conditions induced by non-lesioning doses of kainic acid in the mouse hippocampus, to get insight into the role of zinc under overexcita…

MaleKainic acidSodiumchemistry.chemical_elementAMPA receptorPharmacologyInhibitory postsynaptic potentialHippocampusMicechemistry.chemical_compoundSeizuresmedicineAnimalsPremovement neuronal activityCell damageChelating AgentsNeuronsKainic AcidCell DeathGeneral NeuroscienceGlutamate receptormedicine.diseaseZincnervous systemBiochemistrychemistryNMDA receptorDitiocarbNeuroscience
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Food Intake Adaptation to Dietary Fat Involves PSA-Dependent Rewiring of the Arcuate Melanocortin System in Mice

2012

International audience; Hormones such as leptin and ghrelin can rapidly rewire hypothalamic feeding circuits when injected into rodent brains. These experimental manipulations suggest that the hypothalamus might reorganize continually in adulthood to integrate the metabolic status of the whole body. In this study, we examined whether hypothalamic plasticity occurs in naive animals according to their nutritional conditions. For this purpose, we fed mice with a short-term high-fat diet (HFD) and assessed brain remodeling through its molecular and functional signature. We found that HFD for 3 d rewired the hypothalamic arcuate nucleus, increasing the anorexigenic tone due to activated pro-opio…

MaleMESH: Signal TransductionPro-Opiomelanocortin[ SDV.AEN ] Life Sciences [q-bio]/Food and NutritionSYNAPTIC INPUT ORGANIZATIONMESH: Energy IntakeWeight GainMESH: Mice KnockoutMice0302 clinical medicineMESH : Sialic AcidsNPY/AGRP NEURONSMESH: Pro-OpiomelanocortinMESH: AnimalsMESH : Neuronal PlasticityMESH: Neuronal PlasticityPLASTICITYMESH : Pro-OpiomelanocortinMESH : Adaptation PhysiologicalMice KnockoutFEEDING CIRCUITSMESH : Organ Culture TechniquesINSULIN-RESISTANCE0303 health sciencesNeuronal PlasticityPOLYSIALIC ACIDGeneral NeuroscienceLeptinMESH: Energy Metabolismdigestive oral and skin physiologyINDUCED OBESITYMESH : SialyltransferasesMESH : Weight GainArticlesAdaptation PhysiologicalMESH : Mice TransgenicBODY-WEIGHTMESH: Dietary FatsHypothalamusCELL-ADHESION MOLECULEMESH: Weight GainGhrelinENERGY-BALANCEMelanocortinhormones hormone substitutes and hormone antagonistsSignal Transductionmedicine.medical_specialtyMESH: Mice TransgenicMESH : MaleMESH: SialyltransferasesMESH: Arcuate NucleusMice TransgenicMESH : Mice Inbred C57BLBiologyMESH : Arcuate NucleusMESH: Sialic Acids03 medical and health sciencesOrgan Culture TechniquesInsulin resistanceMESH: Mice Inbred C57BLArcuate nucleusInternal medicineMESH : MicemedicineAnimalsMESH: Mice030304 developmental biologyMESH : Signal TransductionArcuate Nucleus of HypothalamusMESH : Energy Intakemedicine.diseaseDietary FatsMESH: Adaptation PhysiologicalSialyltransferasesMESH: Organ Culture TechniquesMESH: MaleMice Inbred C57BLMESH : Energy MetabolismEndocrinologyMESH: Nerve NetSialic AcidsMESH : Nerve NetMESH : Mice KnockoutMESH : AnimalsNerve NetEnergy IntakeEnergy Metabolism[SDV.AEN]Life Sciences [q-bio]/Food and NutritionMESH : Dietary Fats030217 neurology & neurosurgeryHomeostasisHormoneThe Journal of Neuroscience
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