Search results for "Neuronal"

showing 10 items of 556 documents

Adaptive Function and Brain Evolution

2012

Comparing brains is not a mere intellectual exercise but also helps to understand how the brain enables adaptive behavioral strategies to cope with an ever-changing world and how this complex organ has evolved during the phylogeny. For instance, comparative neurobiology helps understanding the specific features of our species, an issue that attracted scientists since the time of Santiago Ramon y Cajal. Following this tradition, 20 years ago Hans ten Donkelaar and Gerhard Roth started the European Conferences on Comparative Neurobiology (ECCN). This e-book includes some of the contributions to the last meeting, the sixth ECCN (Valencia, Spain; April 22-24 2010), plus selected works by severa…

Brain developmentMathematicsofComputing_GENERALNeuroscience (miscellaneous)GeneralLiterature_MISCELLANEOUSbrainstemlcsh:RC321-571lcsh:QM1-695Adaptive functioningInformationSystems_GENERALCellular and Molecular NeuroscienceComparative Neuroanatomylcsh:Neurosciences. Biological psychiatry. NeuropsychiatryDCN NN - Brain networks and neuronal communicationGeneralLiterature_REFERENCE(e.g.dictionariesencyclopediasglossaries)Cerebral CortexEvolutionary NeuroscienceCognitive scienceBrain DevelopmentEvolutionary neurosciencelcsh:Human anatomyNeuroanatomyEditorialForebrainAnatomyPsychologyClassicsFrontiers in Neuroanatomy
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Immunelectronmicroscopic characterization of T4 and T8 lymphocytes and natural killer cells in neuronal ceroid-lipofuscinosis.

1995

CD4+, CD8+, and CD56+ cells were isolated with the immunomagnetic separation technique from peripheral blood mononuclear cells (PBMC) of 3 patients with neuronal ceroid-lipofuscinosis : one patient each with infantile (INCL), late infantile (LINCL), and juvenile (JNCL) neuronal ceroid-lipofuscinoses, all studied by light (LM) and electron (EM) microscopy. To compare the pathology of these cells with affected cells in other types of lysosomal diseases, the separation was also performed with PBMC of 1 patient with mucolipidosis (ML) type II, 2 patients with mucopolysaccharidosis (MPS) type I, and 4 patients with MPS type III. Disease-specific lysosomal inclusions were identified in CD4+, CD8+…

CD4-Positive T-LymphocytesAdolescentMucolipidosisLymphocyteMucopolysaccharidosisInfantBiologyCD8-Positive T-LymphocytesMucopolysaccharidosesmedicine.diseaseImmunomagnetic separationMolecular biologyPeripheral blood mononuclear cellKiller Cells Naturalmedicine.anatomical_structureNeuronal Ceroid-LipofuscinosesChild PreschoolImmunologymedicineHumansNeuronal ceroid lipofuscinosisLysosomesMicroscopy ImmunoelectronGenetics (clinical)CD8American journal of medical genetics
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Characterization of T–cell subclasses and NK–cells in lysosomal disorders by immuno–electron microscopy

1994

Previous studies have shown that B and T lymphocytes are affected in lysosomal disorders. The aim of this study was to investigate the involvement of subclasses of T lymphocytes and natural killer cells in lysosomal diseases. CD4+, CD8+, and CD56+ cells were immunomagnetically separated from peripheral blood mononuclear cells in 10 patients with various lysosomal diseases--including one patient each with infantile, late infantile, and juvenile neuronal ceroid-lipfuscinoses, two patients with mucopolysaccharidosis (MPS) type I and four patients with MPS type III, and one patient with mucolipidosis type II; all lymphocytes were studied by light and electron microscopy. Respective vacuolar or …

CD4-Positive T-LymphocytesPathologymedicine.medical_specialtyHistologyT-LymphocytesMucopolysaccharidosisT cellImmunoblottingCD8-Positive T-LymphocytesBiologyPathology and Forensic MedicineNatural killer cellPhysiology (medical)Lysosomal storage diseasemedicineHumansMicroscopy ImmunoelectronT lymphocyteMucopolysaccharidosesmedicine.diseaseKiller Cells Naturalmedicine.anatomical_structureNeurologyNeuronal ceroid lipofuscinosisNeurology (clinical)I-cell diseaseLysosomesCD8Neuropathology and Applied Neurobiology
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Intrahippocampal transplantation of mesenchymal stromal cells promotes neuroplasticity

2012

Multipotent mesenchymal stromal cells (MSC) secrete soluble factors that stimulate the surrounding microenvironment. Such paracrine effects might underlie the potential benefits of many stem cell therapies. We tested the hypothesis that MSC are able to enhance intrinsic cellular plasticity in the adult rat hippocampus.Rat bone marrow-derived MSC were labeled with very small superparamagnetic iron oxide particles (VSOP), which allowed for non-invasive graft localization by magnetic resonance imaging (MRI). Moreover, MSC were transduced with lentiviral vectors to express the green fluorescent protein (GFP). The effects of bilateral MSC transplantation on hippocampal cellular plasticity were a…

Cancer ResearchCell SurvivalImmunologyCell- and Tissue-Based TherapyBone Marrow CellsCitalopramHippocampal formationBiologyMesenchymal Stem Cell TransplantationFerric CompoundsHippocampusGreen fluorescent proteinParacrine signallingAnimalsImmunology and AllergyGenetics (clinical)Cell ProliferationTransplantationNeuronal PlasticityCell growthMesenchymal stem cellNeurogenesisMesenchymal Stem CellsCell BiologyAnatomyMagnetic Resonance ImagingRatsCell biologyTransplantationOncologyStem cellCytotherapy
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Membrane vesicles shed by oligodendroglioma cells induce neuronal apoptosis.

2006

In order to investigate the mechanism by which oligodendrogliomas cause neuronal damage, media conditioned by G26/24 oligodendroglioma cells, were fractionated into shed vesicles and vesicle-free supernatants, and added to primary cultures of rat fetal cortical neurons. After one night treatment with vesicles, a reproducible, dose-dependent, inhibitory effect on neurite outgrowth was already induced and, after 48-72 h of incubation, neuronal apoptosis was evident. Vesicle-free supernatants and vesicles shed by NIH-3T3 cells had no inhibitory effects on neurons. Western blot analyses showed that treated neurons expressed a decreased amount of neurofilament (NF), growth-associated protein (GA…

Cancer ResearchCell signalingProgrammed cell deathPathologymedicine.medical_specialtyNeurofilamentFas Ligand ProteinNeuriteCellOligodendrogliomaApoptosisCell CommunicationBiologyRats Sprague-DawleyMiceWestern blotmedicineAnimalsMyelin SheathCerebral CortexNeuronsmedicine.diagnostic_testVesicleCytoplasmic Vesiclesoligodendroglioma membrane vesicles neuronal apoptosis Fas-L Nogo.Cell biologyRatsmedicine.anatomical_structureOncologyNIH 3T3 CellsNeuronInternational journal of oncology
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Resistance to diverse apoptotic triggers in multidrug resistant HL60 cells and its possible relationship to the expression of P-glycoprotein, Fas and…

2002

We studied the human HL60 leukemia cell line and its multidrug resistant (MDR) variant HL60R. In contrast to the HL60, HL60R showed an inability to undergo apoptosis from doxorubicin (Dox) or other different stimuli, including cisplatin, Fas ligation and serum withdrawal. HL60R cells lost surface Fas expression, but we found no evidence that Fas/FasL mediates the apoptotic effects of Dox in HL60. P-glycoprotein (P-gp) did not seem to play a major role as a specific inhibitor of apoptosis. In fact, the P-gp inhibitor verapamil reversed only partially the resistance to Dox-induced apoptosis of the MDR cells. In addition, it did not modify the rate of apoptosis induced from the other stimuli i…

Cancer ResearchProgrammed cell deathTime FactorsChromosomal Proteins Non-HistoneSurvivinDown-RegulationAntineoplastic AgentsApoptosisHL-60 CellsNerve Tissue ProteinsBiologyInhibitor of apoptosisFas ligandInhibitor of Apoptosis ProteinsInhibitory Concentration 50SurvivinTumor Cells CulturedHumansATP Binding Cassette Transporter Subfamily B Member 1RNA Messengerfas ReceptorP-glycoproteinInhibitor of apoptosis domainCaspase 3Reverse Transcriptase Polymerase Chain ReactionProteinsFlow CytometryNeuronal Apoptosis-Inhibitory ProteinNeoplasm ProteinsCell biologyProto-Oncogene Proteins c-bcl-2OncologyDoxorubicinDrug Resistance NeoplasmApoptosisCaspasesbiology.proteinInsect ProteinsNAIPCisplatinMicrotubule-Associated ProteinsCancer Letters
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Functional genomics indicate that schizophrenia may be an adult vascular-ischemic disorder

2015

AbstractIn search for the elusive schizophrenia pathway, candidate genes for the disorder from a discovery sample were localized within the energy-delivering and ischemia protection pathway. To test the adult vascular-ischemic (AVIH) and the competing neurodevelopmental hypothesis (NDH), functional genomic analyses of practically all available schizophrenia-associated genes from candidate gene, genome-wide association and postmortem expression studies were performed. Our results indicate a significant overrepresentation of genes involved in vascular function (P<0.001), vasoregulation (that is, perivascular (P<0.001) and shear stress (P<0.01), cerebral ischemia (P<0.001), neurode…

Candidate genemedicine.medical_specialtyPostmortem studiesLong-Term PotentiationBiologySynaptic TransmissionBrain IschemiaBrain ischemiaCellular and Molecular NeuroscienceInternal medicinemedicineHumansGenetic Predisposition to Diseaseddc:610Biological PsychiatryNeuronal PlasticityNeurogenesisGlutamate receptorLong-term potentiationGenomicsmedicine.diseasePsychiatry and Mental healthEndocrinologySchizophreniaSynaptic plasticitySchizophreniaOriginal ArticleNeuroscienceGenome-Wide Association Study
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The endocannabinoid N-arachidonoyldopamine (NADA) exerts neuroprotective effects after excitotoxic neuronal damage via cannabinoid receptor 1 (CB(1)).

2012

Endocannabinoids exert numerous effects in the CNS under physiological and pathological conditions. The aim of the present study was to examine whether the endocannabinoid N-arachidonoyldopamine (NADA) may protect neurons in excitotoxically lesioned organotypic hippocampal slice cultures (OHSC). OHSC were excitotoxically lesioned by application of N-methyl-d-aspartate (NMDA, 50 μM) for 4 h and subsequently treated with different NADA concentrations (0.1 pM-50 μM) alone or in combination with cannabinoid receptor antagonists. NADA protected dentate gyrus granule cells and caused a slight reduction in the number of microglial cells. The number of degenerated neurons significantly decreased be…

Cannabinoid receptorDopamineTRPV1Arachidonic AcidsPharmacologyNeuroprotectionHippocampusCellular and Molecular NeuroscienceMicePiperidinesReceptor Cannabinoid CB1Neuronal damageAnimalsRats WistarCells CulturedPharmacologyNeuronsChemistryDentate gyrusExcitatory Postsynaptic PotentialsEndocannabinoid systemRatsNeuroprotective Agentsnervous systemNerve DegenerationCannabinoid receptor antagonistNMDA receptorPyrazolesNeuropharmacology
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The endocannabinoid system in anxiety, fear memory and habituation.

2011

Evidence for the involvement of the endocannabinoid system (ECS) in anxiety and fear has been accumulated, providing leads for novel therapeutic approaches. In anxiety, a bidirectional influence of the ECS has been reported, whereby anxiolytic and anxiogenic responses have been obtained after both increases and decreases of the endocannabinoid tone. The recently developed genetic tools have revealed different but complementary roles for the cannabinoid type 1 (CB1) receptor on GABAergic and glutamatergic neuronal populations. This dual functionality, together with the plasticity of CB1 receptor expression, particularly on GABAergic neurons, as induced by stressful and rewarding experiences…

Cannabinoid receptormedicine.drug_classclassical conditioninggamma-aminobutyric acidglutamateAnxietyAnxiolyticstressReceptor Cannabinoid CB1MemoryCannabinoid Receptor ModulatorsmedicineAnimalsHumansneuronal plasticityPharmacology (medical)HabituationendocannabinoidsHabituation PsychophysiologicPharmacologyExtinction (psychology)FearArticleshabituationEndocannabinoid systemPsychiatry and Mental healthAnxiogenicnervous systemcannabinoid CB1 receptorAnxietyMemory consolidationlipids (amino acids peptides and proteins)medicine.symptomPsychologyNeuroscienceJournal of psychopharmacology (Oxford, England)
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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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