Search results for "Cerebral Cortex"

showing 10 items of 529 documents

Protective action of 1,3-butanediol in cerebral ischemia. A neurologic, histologic, and metabolic study.

1987

1,3-Butanediol (BD) is converted in the body to β-hydroxybutyrate, and previous studies have shown that hyperketonemia had beneficial effects in experimental models of generalized hypoxia. The aim of this study was to determine if BD would reduce brain damage following cerebral ischemia. A transient forebrain ischemia of 30-min duration was induced by the four-vessel occlusion technique in control and BD-treated rats (25 mmol/kg, i.p.; 30 min prior to ischemia). BD treatment led to significant improvement of neurologic deficit during the 72-h recovery period and reduced neuronal damage in the striatum and cortex but not in the CA1 sector of the hippocampus. Evaluation of cerebral energy me…

Blood GlucoseMalemedicine.medical_specialtyIschemiaHydroxybutyratesBlood PressureBrain damageHippocampusPhosphocreatinechemistry.chemical_compoundInternal medicinemedicine13-ButanediolAnimalsEnergy chargeButylene GlycolsCerebral CortexNeurons3-Hydroxybutyric Acidbusiness.industryBrainHypoxia (medical)medicine.diseaseCorpus StriatumRatsEndocrinologyNeurologychemistryIschemic Attack TransientLactic acidosisKetone bodiesNeurology (clinical)medicine.symptomCardiology and Cardiovascular MedicinebusinessEnergy MetabolismJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism
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A Neuroprotective Function for the Hematopoietic Protein Granulocyte-Macrophage Colony Stimulating Factor (GM-CSF)

2007

Granulocyte-macrophage colony-stimulating factor (GM-CSF) is a hematopoietic cytokine responsible for the proliferation, differentiation, and maturation of cells of the myeloid lineage, which was cloned more than 20 years ago. Here we uncovered a novel function of GM-CSF in the central nervous system (CNS). We identified the GM-CSF α-receptor as an upregulated gene in a screen for ischemia-induced genes in the cortex. This receptor is broadly expressed on neurons throughout the brain together with its ligand and induced by ischemic insults. In primary cortical neurons and human neuroblastoma cells, GM-CSF counteracts programmed cell death and induces BCL-2 and BCL-Xl expression in a dose- a…

Brain InfarctionMaleProgrammed cell deathTime FactorsMyeloidmedicine.medical_treatmentDrug Evaluation Preclinicalbcl-X ProteinApoptosisBiologyNeuroprotectionBrain IschemiaPhosphatidylinositol 3-KinasesmedicineAnimalsHumansMyeloid CellsRats Long-EvansRats WistarProtein kinase BCell ProliferationCerebral CortexNeuronsDose-Response Relationship DrugGrowth factorGranulocyte-Macrophage Colony-Stimulating FactorCell DifferentiationNeurodegenerative DiseasesRatsUp-RegulationCell biologyDisease Models AnimalHaematopoiesisNeuroprotective Agentsmedicine.anatomical_structureGranulocyte macrophage colony-stimulating factorNeurologyBlood-Brain BarrierReceptors Granulocyte-Macrophage Colony-Stimulating FactorImmunologyNeurology (clinical)Signal transductionCardiology and Cardiovascular MedicineProto-Oncogene Proteins c-aktSignal Transductionmedicine.drugJournal of Cerebral Blood Flow & Metabolism
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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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Les Réponses évoquées Du Noyau Caudé A La Suite De Modifications De L'Excitabilité De L'Aire Auditive Primaire

1966

CATSPhysiologybusiness.industryAuditory areaCaudate nucleusStrychnineBiochemistryTemporal lobeElectrophysiologychemistry.chemical_compoundmedicine.anatomical_structurechemistryCerebral cortexMedicinebusinessNeuroscienceArchives Internationales de Physiologie et de Biochimie
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Experimental „Luxury Perfusion” in the Cerebral Cortex of the Cat

1968

Publisher Summary Preliminary studies have been performed, on the changes of cortical rCBF (Krypton- 85 Beta clearance technique) in response to a localized pressure applied to the cerebral cortex (suprasylvian gyrus) of 8 cats under Nembutal anesthesia (30 to 40 mg/kg bodyweight). No change in rCBF is found at regions as distant as the contralateral hemisphere. The increase of rCBF at the compressed site, during the compression, seems to be more marked in animals with higher blood (i.e. perfusion) pressure, and may be absent in cats with blood pressure of about 80 mm Hg. The augmentation of rCBF around the compressed area during the compression is always very marked, and after some time fl…

CATSbusiness.industryContralateral hemisphereCompression (physics)medicine.anatomical_structureBlood pressureGyrusCerebral cortexAnesthesiamedicineLuxury perfusionbusinessNuclear medicinePerfusion
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Rebalancing β-Amyloid-Induced Decrease of ATP Level by Amorphous Nano/Micro Polyphosphate: Suppression of the Neurotoxic Effect of Amyloid β-Protein …

2017

Morbus Alzheimer neuropathology is characterized by an impaired energy homeostasis of brain tissue. We present an approach towards a potential therapy of Alzheimer disease based on the high-energy polymer inorganic polyphosphate (polyP), which physiologically occurs both in the extracellular and in the intracellular space. Rat pheochromocytoma (PC) 12 cells, as well as rat primary cortical neurons were exposed to the Alzheimer peptide Aβ25-35. They were incubated in vitro with polyphosphate (polyP); ortho-phosphate was used as a control. The polymer remained as Na+ salt; or complexed in a stoichiometric ratio to Ca2+ (Na-polyP[Ca2+]); or was processed as amorphous Ca-polyP microparticles (C…

Calcium Phosphates0301 basic medicineIntracellular SpacePeptidelcsh:Chemistrychemistry.chemical_compoundAdenosine TriphosphateX-Ray DiffractionPolyphosphatesSpectroscopy Fourier Transform Infraredprimary rat cortex neuronslcsh:QH301-705.5SpectroscopyCerebral CortexNeuronschemistry.chemical_classificationmicroparticlesChemistryβ-amyloidGeneral Medicinepathological conditions signs and symptomsComputer Science Applicationsneurotoxic effectsurgical procedures operativeBiochemistryAlzheimer's diseaseIntracellularCell Survivalβ-amyloid; calcium polyphosphate; microparticles; neurotoxic effect; adenosine triphosphate level; PC12 cells; primary rat cortex neuronsArticleCatalysisInorganic Chemistry03 medical and health sciencesmedicineExtracellularotorhinolaryngologic diseasesAnimalsPhysical and Theoretical ChemistryMolecular BiologyneoplasmsAmyloid beta-PeptidesPolyphosphateOrganic ChemistryNeurotoxicityPC12 cellsmedicine.diseaseIn vitrodigestive system diseasesRats030104 developmental biologylcsh:Biology (General)lcsh:QD1-999BiophysicsNanoparticlesAdenosine triphosphatecalcium polyphosphateadenosine triphosphate levelInternational Journal of Molecular Sciences
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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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WIN 55,212-2, agonist of cannabinoid receptors, prevents amyloid β1-42 effects on astrocytes in primary culture

2015

Alzheimer's disease (AD), a neurodegenerative illness involving synaptic dysfunction with extracellular accumulation of Aβ1-42 toxic peptide, glial activation, inflammatory response and oxidative stress, can lead to neuronal death. Endogenous cannabinoid system is implicated in physiological and physiopathological events in central nervous system (CNS), and changes in this system are related to many human diseases, including AD. However, studies on the effects of cannabinoids on astrocytes functions are scarce. In primary cultured astrocytes we studied cellular viability using MTT assay. Inflammatory and oxidative stress mediators were determined by ELISA and Western-blot techniques both in…

Cannabinoid receptormedicine.medical_treatmentInterleukin-1betaNitric Oxide Synthase Type IIlcsh:Medicinemedicine.disease_causeReceptors CannabinoidWIN 55212-2Receptorlcsh:ScienceCerebral CortexMultidisciplinaryCalcium Channel BlockersSistema nerviós Malaltiesmedicine.symptomSignal transductionResearch ArticleSignal Transductionmedicine.drugmedicine.medical_specialtyCell SurvivalMorpholinesPrimary Cell CultureInflammationNaphthalenesBiologyNeurologiaFetusInternal medicinemedicineAnimalsViability assayCannabinoid Receptor AgonistsAmyloid beta-PeptidesSuperoxide DismutaseTumor Necrosis Factor-alphalcsh:RTranscription Factor RelAPeptide FragmentsBenzoxazinesRatsPPAR gammaOxidative StressEndocrinologyGene Expression RegulationCyclooxygenase 2Astrocyteslcsh:QFisiologia humanaCannabinoidOxidative stress
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Tetanus Toxin Inhibits Neuroexocytosis Even When Its Zn2+-dependent Protease Activity Is Removed

1995

Tetanus toxin (TeTX) is a dichain protein that blocks neuroexocytosis, an action attributed previously to Zn(2+)-dependent proteolysis of synaptobrevin (Sbr) by its light chain (LC). Herein, its cleavage of Sbr in rat cerebrocortical synaptosomes was shown to be minimized by captopril, an inhibitor of certain metalloendoproteases, whereas this agent only marginally antagonized the inhibition of noradrenaline release, implicating a second action of the toxin. This hypothesis was proven by preparing three mutants (H233A, E234A, H237A) of the LC lacking the ability to cleave Sbr and reconstituting them with native heavy chain. The resultant dichains were found to block synaptosomal transmitter…

CaptoprilSynaptobrevinProteolysismedicine.medical_treatmentGuinea PigsInhibitory postsynaptic potentialmedicine.disease_causeBiochemistryExocytosisNorepinephrinechemistry.chemical_compoundTetanus ToxinCadaverineAplysiaEndopeptidasesmedicineAnimalsEnzyme InhibitorsNeurotransmitterMolecular BiologyCerebral CortexTransglutaminasesProteasemedicine.diagnostic_testbiologyToxinHydrolysisWild typeCell Biologybiology.organism_classificationRecombinant ProteinsRatsZincBiochemistrychemistryAplysiaBiophysicsSynaptosomesJournal of Biological Chemistry
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Carbachol-induced network oscillations in the intact cerebral cortex of the newborn rat.

2003

In mature cortex, activation of the cholinergic system induces oscillatory network activity and facilitates synaptic plasticity. We used an in vitro preparation of the intact cerebral cortex and cortical slices of the neonatal rat to study carbachol (CCh, >or=30 micro M)-induced network oscillations during the early postnatal period. Multi-site extracellular recordings revealed CCh-induced transient beta oscillations with an average duration of 4.6 +/- 0.2 s, amplitude of 123 +/- 7.4 microV and frequency of 17.7 +/- 0.5 Hz. These oscillations propagated uniformly at 0.5-1.5 mm/s over the cortex and were reversibly blocked by tetrodotoxin (TTX) and atropine, indicating that they depended on …

CarbacholCognitive NeuroscienceKainate receptorAMPA receptorIn Vitro TechniquesCellular and Molecular Neurosciencechemistry.chemical_compoundBiological ClocksCortex (anatomy)medicineAnimalsRats WistarCerebral CortexRatsmedicine.anatomical_structurechemistryAnimals NewbornCholinergic FibersCerebral cortexCNQXBiophysicsGabazineNMDA receptorCarbacholNerve NetNeurosciencemedicine.drugCerebral cortex (New York, N.Y. : 1991)
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