Search results for "ASTROCYTES"

showing 10 items of 171 documents

Sodium dynamics: another key to astroglial excitability?

2012

Astroglial excitability is largely mediated by fluctuations in intracellular ion concentrations. In addition to generally acknowledged Ca 2+ excitability of astroglia, recent studies have demonstrated that neuronal activity triggers transient increases in the cytosolic Na + concentration ([Na + ] i ) in perisynaptic astrocytes. These [Na + ] i transients are controlled by multiple Na + -permeable channels and Na + -dependent transporters; spatiotemporally organized [Na + ] i dynamics in turn regulate diverse astroglial homeostatic responses such as metabolic/signaling utilization of lactate and glutamate, transmembrane transport of neurotransmitters and K + buffering. In particular, near-me…

NeuronsSodium-calcium exchangerbiologyChemistryGeneral NeuroscienceSodiumGlutamate receptorBrainCell CommunicationNeurotransmissionMembrane transportSynaptic TransmissionSodium-Calcium ExchangerCell biologySynapsenervous systemAstrocytesbiology.proteinAnimalsHumansGABA transporterSodium-Potassium-Exchanging ATPaseNa+/K+-ATPaseIntracellularTrends in Neurosciences
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Oligodendrocyte ablation triggers central pain independently of innate or adaptive immune responses in mice.

2014

Mechanisms underlying central neuropathic pain are poorly understood. Although glial dysfunction has been functionally linked with neuropathic pain, very little is known about modulation of pain by oligodendrocytes. Here we report that genetic ablation of oligodendrocytes rapidly triggers a pattern of sensory changes that closely resemble central neuropathic pain, which are manifest before overt demyelination. Primary oligodendrocyte loss is not associated with autoreactive T- and B-cell infiltration in the spinal cord and neither activation of microglia nor reactive astrogliosis contribute functionally to central pain evoked by ablation of oligodendrocytes. Instead, light and electron micr…

NociceptionSpinothalamic tractSpinal Cord Dorsal HornSpinothalamic TractsT-LymphocytesGeneral Physics and AstronomyAdaptive ImmunityGeneral Biochemistry Genetics and Molecular BiologyArticleMicemedicineAnimalsOligodendrocyte; central painB-LymphocytesMultidisciplinaryMicrogliabusiness.industryGeneral Chemistrymedicine.diseaseSpinal cordOligodendrocyteAxonsImmunity InnateAstrogliosisMicroscopy ElectronOligodendrogliamedicine.anatomical_structureNociceptionSpinal CordAstrocytesNeuropathic painNeuralgiaNeuralgiaMicrogliabusinessNeuroscienceNature communications
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“Super p53” Mice Display Retinal Astroglial Changes

2013

Tumour-suppressor genes, such as the p53 gene, produce proteins that inhibit cell division under adverse conditions, as in the case of DNA damage, radiation, hypoxia, or oxidative stress (OS). The p53 gene can arrest proliferation and trigger death by apoptosis subsequent to several factors. In astrocytes, p53 promotes cell-cycle arrest and is involved in oxidative stress-mediated astrocyte cell death. Increasingly, astrocytic p53 is proving fundamental in orchestrating neurodegenerative disease pathogenesis. In terms of ocular disease, p53 may play a role in hypoxia due to ischaemia and may be involved in the retinal response to oxidative stress (OS). We studied the influence of the p53 ge…

PathologyAnatomy and PhysiologyCell divisionMouselcsh:MedicineFluorescent Antibody Techniquemedicine.disease_causechemistry.chemical_compoundMiceMolecular Cell Biologylcsh:ScienceMultidisciplinaryGlial fibrillary acidic proteinAnimal ModelsCell biologymedicine.anatomical_structureMedicineOftalmologíaDNA modificationAstrocyteResearch ArticleSignal TransductionProgrammed cell deathmedicine.medical_specialtyCell PhysiologyHistologyOcular AnatomyNeurocienciasMice TransgenicBiologyRetinaModel OrganismsOcular SystemGlial Fibrillary Acidic ProteinmedicineGeneticsAnimalsBiologyRetinaStaining and Labelinglcsh:RRetinalAnatomía ocularMice Inbred C57BLGenética médicaOphthalmologychemistryApoptosisAstrocytesbiology.proteinlcsh:QGene expressionGene FunctionTumor Suppressor Protein p53Animal GeneticsOxidative stress
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Swelling, Acidosis, and Irreversible Damage of Glial Cells from Exposure to Arachidonic Acid in vitro

1994

Swelling and damage of C6 glioma cells and of primary cultured astrocytes were analyzed in vitro during incubation with arachidonic acid (AA; 20:4). The cells were suspended in a physiological medium supplemented with AA at concentrations of 0.001–1.0 m M. Cell swelling was quantified by flow cytometry with hydrodynamic focusing. Flow cytometry was also utilized for assessment of cell viability by exclusion of the fluorescent dye propidium iodide and for measurement of the intracellular pH (pHi) by 2′,7′-bis-(2-carboxyethyl)−5(and −6)carboxyfluorescein. Administration of AA caused an immediate dose-dependent swelling of C6 glioma cells, even at a concentration of 0.01 m M. At this level cel…

Pathologymedicine.medical_specialtyCell SurvivalLinoleic acidIntracellular pHBiologychemistry.chemical_compoundTumor Cells CulturedmedicineLactic AcidViability assayPropidium iodideCell damageArachidonic AcidFatty AcidsSodiumHydrogen-Ion Concentrationmedicine.diseaseMolecular biologyNeurologychemistryCell cultureAstrocytesLactatesSteroidsArachidonic acidNeurology (clinical)Swellingmedicine.symptomAcidosisCardiology and Cardiovascular MedicineNeurogliaJournal of Cerebral Blood Flow & Metabolism
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Refining in vitro neurotoxicity testing--the development of blood-brain barrier models.

2003

The purpose of this paper is to review the current state of development of advanced in vitro blood–brain barrier (BBB) models. The BBB is a special capillary bed that separates the blood from the central nervous system (CNS) parenchyma. Astrocytes maintain the integrity of the BBB, and, without astrocytic contacts, isolated brain capillary endothelial cells in culture lose their barrier characteristics. Therefore, when developing in vitro BBB models, it is important to add astrocytic factors into the culture system. Recently, novel filter techniques and co-culture methods have made it possible to develop models which resemble the in vivo functions of the BBB in an effective way. With a BBB…

Pathologymedicine.medical_specialtyIn Vitro TechniquesBiologyIn Vitro TechniquesToxicologyBlood–brain barrierModels BiologicalGeneral Biochemistry Genetics and Molecular BiologyIn vivoToxicity TestsmedicinePharmacokineticsCells CulturedNeurotoxicityEndothelial CellsGeneral MedicineIsolated brainmedicine.diseaseCell biologyEndothelial stem cellMedical Laboratory Technologymedicine.anatomical_structurenervous systemBlood-Brain BarrierAstrocytescardiovascular systemNeuronAstrocyteAlternatives to laboratory animals : ATLA
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Neuronal and BBB damage induced by sera from patients with secondary progressive multiple sclerosis.

2009

An important component of the pathogenic process of multiple sclerosis (MS) is the blood-brain barrier (BBB) damage. We recently set an in vitro model of BBB, based on a three-cell-type co-culture system, in which rat neurons and astrocytes synergistically induce brain capillary endothelial cells to form a monolayer with permeability properties resembling those of the physiological BBB. Herein we report that the serum from patients with secondary progressive multiple sclerosis (SPMS) has a damaging effect on isolated neurons. This finding suggests that neuronal damaging in MS could be a primary event and not only secondary to myelin damage, as generally assumed. SPMS serum affects the perme…

Pathologymedicine.medical_specialtyProgrammed cell deathBlotting WesternBiologyImmunofluorescenceOccludinModels BiologicalMyelinWestern blotOccludinGeneticsmedicineElectric ImpedanceAnimalsmultiple sclerosis brain cell cultures in vitro models of blood-brain barrier neuronal cell death transendothelial electrical resistanceMicroscopy Phase-ContrastRats WistarCells CulturedNeuronsmedicine.diagnostic_testTight junctionCell DeathMultiple sclerosisMembrane ProteinsGeneral MedicineMultiple Sclerosis Chronic Progressivemedicine.diseaseImmunohistochemistryRatsBlotmedicine.anatomical_structurenervous systemBlood-Brain BarrierAstrocytescardiovascular systemInternational journal of molecular medicine
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Possible Role of Glymphatic System of the Brain in the Pathogenesis of High-Altitude Cerebral Edema

2018

Simka, Marian, Paweł Latacz, and Joanna Czaja. Possible role of glymphatic system of the brain in the pathogenesis of high-altitude cerebral edema. High Alt Med Biol. 19:394–397, 2018.—In this article, we suggest that the glymphatic system of the brain can play an important role in the pathogenesis of high-altitude cerebral edema (HACE). Water enters the intercellular space of the brain primarily through aquaporin-4 (AQP-4) water channels, the main component of the glymphatic system, whereas acetazolamide, pharmacological agent used in the prevention of HACE, is the blocker of the AQP-4 molecule. In animal experiments, cerebral edema caused by hypobaric hypoxia was associated with an increa…

Physiologyglymphatic systemaquaporin-4Brain EdemaAltitude Sickness030204 cardiovascular system & hematologyCerebral edemaPathogenesis03 medical and health sciences0302 clinical medicinemedicineAnimalsHumansAquaporin 4business.industryAltitudePublic Health Environmental and Occupational HealthastrocytesBrainGeneral MedicineEffects of high altitude on humansmedicine.diseaseSleep in non-human animalsAcetazolamideAquaporin 4Glymphatic systemAcetazolamidebusinessNeuroscience030217 neurology & neurosurgeryHigh-altitude cerebral edemamedicine.drug
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3D cultures of rat astrocytes and brain capillary endothelial cells on Poly-L-lactic acid scaffolds

2016

Tissue engineering is an emerging multidisciplinary field that aims at reproducing in vitro and/or in vivo tissues with morphological and functional features similar to the biological tissue of the human body. In this communication we report setting of three-dimensional structures able to mimic the extracellular matrix of the nervous system: we prepared Poly-L-Lactic Acid (PLLA) porous scaffolds via thermally induced phase separation (TIPS), and investigated the parameters that influence porosity, average pore size and degree of interconnection, i.e. polymer concentration, temperature and time of process. Astrocytes and brain capillary endothelial cells (BCECs) were cultured on these three-…

Poly-L-Lactic Acid (PLLA) porous scaffolds Astrocytes brain capillary endothelial cells (BCECs) 2D culture systems and 3D culture systemsSettore ING-IND/22 - Scienza E Tecnologia Dei MaterialiSettore BIO/13 - Biologia ApplicataSettore BIO/10 - BiochimicaSettore BIO/06 - Anatomia Comparata E Citologia
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Oligodendrocytes in mouse corpus callosum are coupled via gap junction channels formed by connexin47 and connexin32.

2010

According to previously published ultrastructural studies, oligodendrocytes in white matter exhibit gap junctions with astrocytes, but not among each other, while in vitro oligodendrocytes form functional gap junctions. We have studied functional coupling among oligodendrocytes in acute slices of postnatal mouse corpus callosum. By whole-cell patch clamp we dialyzed oligodendrocytes with biocytin, a gap junction-permeable tracer. On average 61 cells were positive for biocytin detected by labeling with streptavidin-Cy3. About 77% of the coupled cells stained positively for the oligodendrocyte marker protein CNPase, 9% for the astrocyte marker GFAP and 14% were negative for both CNPase and GF…

PolydendrocytesPatch-Clamp TechniquesPopulationNerve Tissue ProteinsBiologyIn Vitro TechniquesConnexinsCorpus CallosumOLIG2Cellular and Molecular Neurosciencechemistry.chemical_compoundMyelinMiceBiocytinGlial Fibrillary Acidic ProteinmedicineBasic Helix-Loop-Helix Transcription FactorsConnexin 30AnimalsAntigenseducationMice Knockouteducation.field_of_studyLysineStem CellsGap junctionGap JunctionsCarbocyaninesOligodendrocyte Transcription Factor 2OligodendrocyteCell biologyMice Inbred C57BLOligodendrogliamedicine.anatomical_structureNeurologychemistryAstrocytesProteoglycansStreptavidin2'3'-Cyclic-Nucleotide PhosphodiesterasesNeuroscienceAstrocyteGlia
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Cytoprotective effect of NMDA receptor antagonists on prion protein (PrionSc)-induced toxicity in rat cortical cell cultures

1993

Rat cortical cells were incubated with the Scrapie prion protein, PrionSc. At concentrations of 3 ng/ml of PrionSc and higher, the viability of the cells decreased significantly after a 12-h incubation period. Simultaneously, the degree of DNA fragmentation increased. In control experiments with antibodies against PrionSc, PrionSc lost its deleterious effect on neurons. PrionSc did not affect the viability of astrocytes. Drugs known to block NMDA receptor channels, such as memantine (1-amino-3,5-dimethyl-adamantane) (Mem), its analogue 1-N-methylamino-3,5-dimethyl-adamantane as well as (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine maleate (MK-801) prevented the effect of …

PrPSc ProteinsCell SurvivalPrionsNerve Tissue ProteinsScrapiePharmacologyReceptors N-Methyl-D-AspartateIncubation periodNeuroblastomaTumor Cells CulturedmedicineAnimalsRats WistarCells CulturedCerebral CortexNeuronsPharmacologybiologyMemantineCalcium Channel BlockersIn vitroRatsAstrocytesLiposomesToxicityImmunologybiology.proteinDNA fragmentationNMDA receptorAntibodymedicine.drugEuropean Journal of Pharmacology: Molecular Pharmacology
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