Search results for "Pyramidal Cells"

showing 10 items of 45 documents

Optical release of caged glutamate for stimulation of neurons in the in vitro slice preparation

2005

Optical stimulation techniques prove useful to map func- tional inputs in the in vitro brain slice preparation: Glutamate released by a focused beam of UV light induces action potentials, which can be detected in postsynaptic neurons. The direct activation effect is influenced by factors such as compound concentration, focus depth, light absorption in the tissue, and sensitivity of different neuronal do- mains. We analyze information derived from direct stimulation ex- periments in slices from rat barrel cortex and construct a computa- tional model of a layer V pyramidal neuron that reproduces the experimental findings. The model predictions concerning the influ- ence of focus depth on inpu…

MalePatch-Clamp TechniquesUltraviolet RaysModels NeurologicalBiomedical EngineeringAction PotentialsStimulationIn Vitro TechniquesCaged glutamateBrain mappingBiomaterialsOpticsSlice preparationGlutamatesPostsynaptic potentialmedicineAnimalsComputer SimulationRats WistarMicroscopy VideoPhotolysisbusiness.industryChemistryPyramidal CellsGlutamate receptorEquipment DesignSomatosensory CortexBarrel cortexAtomic and Molecular Physics and OpticsRatsElectronic Optical and Magnetic Materialsmedicine.anatomical_structureLens (anatomy)SynapsesBiophysicsbusinessJournal of Biomedical Optics
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Switching between persistent firing and depolarization block in individual rat CA1 pyramidal neurons

2018

The hippocampal formation plays a role in mnemonic tasks and epileptic discharges in vivo. In vitro, these functions and malfunctions may relate to persistent firing (PF) and depolarization block (DB), respectively. Pyramidal neurons of the CA1 field have previously been reported to engage in either PF or DB during cholinergic stimulation. However, it is unknown whether these cells constitute disparate populations of neurons. Furthermore, it is unclear which cell-specific peculiarities may mediate their diverse response properties. However, it has not been shown whether individual CA1 pyramidal neurons can switch between PF and DB states. Here, we used whole cell patch clamp in the current …

MalePotassium ChannelsPatch-Clamp Techniquesantagonists & inhibitors [TRPC Cation Channels]physiology [Electrophysiological Phenomena]Cognitive Neurosciencepharmacology [Muscarinic Agonists]metabolism [TRPC Cation Channels]drug effects [Pyramidal Cells]HippocampusStimulationMuscarinic AgonistsIn Vitro TechniquesHippocampal formation050105 experimental psychologyMembrane Potentialspharmacology [Carbachol]03 medical and health sciences0302 clinical medicineCurrent clampAnimalsRats Long-Evans0501 psychology and cognitive sciencesddc:610Patch clampCA1 Region HippocampalTRPC Cation Channelsphysiology [CA1 Region Hippocampal]Dose-Response Relationship Drugphysiology [Pyramidal Cells]ChemistryPyramidal Cells05 social sciencescytology [CA1 Region Hippocampal]drug effects [Membrane Potentials]Depolarizationmetabolism [Potassium Channels]drug effects [Electrophysiological Phenomena]Potassium channelElectrophysiological PhenomenaRatsdrug effects [CA1 Region Hippocampal]CholinergicCarbacholFemaleNeuroscience030217 neurology & neurosurgeryHippocampus
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Intrinsically determined cell death of developing cortical interneurons.

2009

The cell death of inhibitory neurons, which originate far from the cortical areas to which they migrate during embryonic development, is determined autonomously rather than by competition for trophic signals from other cell types. It has long been known that apoptosis, a form of programmed cell death, eliminates young cells from developing tissues. In the field of neurobiology, it is widely believed that developmental neuronal-cell death results from cellular competition for environmentally derived survival signals that selects for an optimally sized and properly wired population of neurons. This study of developmental cell death in the mouse cortex in vivo, in vitro and after transplantati…

MaleProgrammed cell deathInterneurongenetic structuresCell SurvivalPopulationApoptosisCell CountNeocortexBiologyArticle03 medical and health sciencesMice0302 clinical medicineNeural Stem CellsInterneuronsmedicineAnimalseducationCellular Senescence030304 developmental biologybcl-2-Associated X Protein0303 health scienceseducation.field_of_studyMultidisciplinaryNeocortexMembrane GlycoproteinsCaspase 3musculoskeletal neural and ocular physiologyPyramidal CellsfungiProtein-Tyrosine KinasesCell biologyTransplantationMice Inbred C57BLmedicine.anatomical_structurenervous systemAnimals NewbornInhibitory Postsynaptic PotentialsCerebral cortexbiology.proteinFemaleCell aging030217 neurology & neurosurgeryNeurotrophinNature
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Oligodendrocyte precursor cells modulate the neuronal network by activity-dependent ectodomain cleavage of glial NG2.

2014

The role of glia in modulating neuronal network activity is an important question. Oligodendrocyte precursor cells (OPC) characteristically express the transmembrane proteoglycan nerve-glia antigen 2 (NG2) and are unique glial cells receiving synaptic input from neurons. The development of NG2+ OPC into myelinating oligodendrocytes has been well studied, yet the retention of a large population of synapse-bearing OPC in the adult brain poses the question as to additional functional roles of OPC in the neuronal network. Here we report that activity-dependent processing of NG2 by OPC-expressed secretases functionally regulates the neuronal network. NG2 cleavage by the α-secretase ADAM10 yields…

MaleQH301-705.5ADAM10Long-Term PotentiationAMPA receptorReceptors N-Methyl-D-AspartateGeneral Biochemistry Genetics and Molecular BiologyCell LineADAM10 ProteinMiceBiological neural networkAnimalsBiology (General)AntigensMice KnockoutNeuronsNeuronal PlasticityGeneral Immunology and MicrobiologybiologyGeneral NeurosciencePyramidal CellsGlutamate receptorMembrane ProteinsBiology and Life SciencesLong-term potentiationSensory GatingCell biologyExtracellular MatrixProtein Structure Tertiarystomatognathic diseasesADAM ProteinsOligodendrogliaBiochemistryEctodomainnervous systemReceptors GlutamateSynapsesbiology.proteinSynopsisNMDA receptorProteoglycansAmyloid Precursor Protein SecretasesGeneral Agricultural and Biological SciencesAmyloid precursor protein secretaseNeurosciencePLoS biology
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Depletion of polysialic acid from neural cell adhesion molecule (PSA-NCAM) increases CA3 dendritic arborization and increases vulnerability to excito…

2012

Chronic immobilization stress (CIS) shortens apical dendritic trees of CA3 pyramidal neurons in the hippocampus of the male rat, and dendritic length may be a determinant of vulnerability to stress. Expression of the polysialylated form of neural cell adhesion molecule (PSA-NCAM) in the hippocampal formation is increased by stress, while PSA removal by Endo-neuraminidase-N (endo-N) is known to cause the mossy fibers to defasciculate and synapse ectopically in their CA3 target area. We show here that enzymatic removal of PSA produced a remarkable expansion of dendritic arbors of CA3 pyramidal neurons, with a lesser effect in CA1. This expansion eclipsed the CIS-induced shortening of CA3 dend…

MaleSilver StainingKainic acidExcitotoxicityHippocampusBiologyHippocampal formationmedicine.disease_causeReceptors N-Methyl-D-AspartateArticleBody Mass IndexRats Sprague-DawleySynapsechemistry.chemical_compoundDevelopmental NeuroscienceExcitatory Amino Acid AgonistsmedicineAnimalsOrganic ChemicalsReceptorNeural Cell Adhesion MoleculesAnalysis of VarianceKainic AcidPolysialic acidPyramidal CellsMetalloendopeptidasesDendritesFluoresceinsCA3 Region HippocampalRatsCell biologyDisease Models AnimalGene Expression Regulationnervous systemNeurologychemistryNerve DegenerationSialic AcidsNeural cell adhesion moleculeNeuroscienceStress PsychologicalExperimental Neurology
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The endocannabinoid system controls key epileptogenic circuits in the hippocampus.

2006

SummaryBalanced control of neuronal activity is central in maintaining function and viability of neuronal circuits. The endocannabinoid system tightly controls neuronal excitability. Here, we show that endocannabinoids directly target hippocampal glutamatergic neurons to provide protection against acute epileptiform seizures in mice. Functional CB1 cannabinoid receptors are present on glutamatergic terminals of the hippocampal formation, colocalizing with vesicular glutamate transporter 1 (VGluT1). Conditional deletion of the CB1 gene either in cortical glutamatergic neurons or in forebrain GABAergic neurons, as well as virally induced deletion of the CB1 gene in the hippocampus, demonstrat…

MaleVesicular glutamate transporter 1HUMDISEASEHippocampusGene ExpressionHippocampal formationHippocampusMembrane Potentialschemistry.chemical_compoundMice0302 clinical medicineReceptor Cannabinoid CB1Premovement neuronal activitygamma-Aminobutyric Acid0303 health sciencesKainic AcidbiologyBehavior AnimalReverse Transcriptase Polymerase Chain Reactionmusculoskeletal neural and ocular physiologyGeneral NeurosciencePyramidal CellsCalcium Channel BlockersEndocannabinoid systemlipids (amino acids peptides and proteins)psychological phenomena and processesmedicine.drugKainic acidNeuroscience(all)MorpholinesGlutamic AcidMice TransgenicNaphthalenesMOLNEUROgamma-Aminobutyric acid03 medical and health sciencesGlutamatergicCannabinoid Receptor ModulatorsmedicineAnimals030304 developmental biologyAnalysis of VarianceEpilepsyBenzoxazinesMice Inbred C57BLnervous systemchemistryCalcium-Calmodulin-Dependent Protein KinasesVesicular Glutamate Transport Protein 1biology.proteinNerve NetSYSNEUROCalcium-Calmodulin-Dependent Protein Kinase Type 2Neuroscience030217 neurology & neurosurgeryEndocannabinoidsNeuron
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Dendritic Ih selectively blocks temporal summation of unsynchronized distal inputs in CA1 pyramidal neurons.

2004

The active dendritic conductances shape the input-output properties of many principal neurons in different brain regions, and the various ways in which they regulate neuronal excitability need to be investigated to better understand their functional consequences. Using a realistic model of a hippocampal CA1 pyramidal neuron, we show a major role for the hyperpolarization-activated current, I-h, in regulating the spike probability of a neuron when independent synaptic inputs are activated with different degrees of synchronization and at different distances from the soma. The results allowed us to make the experimentally testable prediction that the I-h in these neurons is needed to reduce ne…

N-MethylaspartateTime FactorsComputer scienceCognitive NeuroscienceModels NeurologicalNeural ConductionHippocampal formationSummationHippocampusSynaptic TransmissionCA1Cellular and Molecular NeurosciencemedicineExcitatory Amino Acid AgonistsAnimalsComputer Simulationalpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic AcidI-hProbabilityCa1 pyramidal neuronPyramidal CellsExcitatory Postsynaptic PotentialsReproducibility of ResultsmodelingDendritesSensory Systemsdendritic integrationmedicine.anatomical_structurenervous systemSomaNeuronNeuroscience
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Cell expression of GDAP1 in the nervous system and pathogenesis of Charcot-Marie-Tooth type 4A disease

2007

Abstract Mutations in the mitochondrial protein GDAP1 are the cause of Charcot-Marie-Tooth type 4A disease (CMT4A), a severe form of peripheral neuropathy associated with either demyelinating, axonal or intermediate pheno-types. GDAP1 is located in the outer mitochondrial membrane and it seems that may be related with the mitochondrial network dynamics. We are interested to define cell expression in the nervous system and the effect of mutations in mitochondrial morphology and pathogenesis of the disease. We investigated GDAP1 expression in the nervous system and dorsal root ganglia (DRG) neuron cultures. GDAP1 is expressed in motor and sensory neurons of the spinal cord and other large neu…

Nervous systemCMT4A mutations and pathogenesisPathologymedicine.medical_specialtyperipheral neuropathyCharcot-Marie-Tooth type 4A diseaseMutation MissenseGene ExpressionImages in Cellular / Molecular MedicineNerve Tissue ProteinsGDAP1MitochondrionBiologymedicine.disease_causeNervous SystemPathogenesisMicePurkinje CellsCharcot-Marie-Tooth DiseaseInterneuronsGanglia SpinalChlorocebus aethiopsmedicineAnimalsHumansNeurons AfferentCells CulturedMotor NeuronsMutationfusion and fission pathwayPyramidal CellsCell Biologymedicine.diseaseSpinal cordImmunohistochemistrymitochondrial dynamicsCell biologyOlfactory bulbRatsmedicine.anatomical_structurePeripheral neuropathynervous systemAnimals NewbornSpinal CordCOS CellsMolecular MedicineNeuronHeLa CellsJournal of Cellular and Molecular Medicine
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Monoclonal antibodies SMI 311 and SMI 312 as tools to investigate the maturation of nerve cells and axonal patterns in human fetal brain

1998

Neurofilaments, which are exclusively found in nerve cells, are one of the earliest recognizable features of the maturing nervous system. The differential distribution of neurofilament proteins in varying degrees of phosphorylation within a neuron provides the possibility of selectively demonstrating either somata and dendrites or axons. Non-phosphorylated neurofilaments typical of somata and dendrites can be visualized with the aid of monoclonal antibody SMI 311, whereas antibody SMI 312 is directed against highly phosphorylated axonal epitopes of neurofilaments. The maturation of neuronal types, the development of area-specific axonal networks, and the gradients of maturation can thus be …

Nervous systemHistologyNeurofilamentmedicine.drug_classeducationImmunocytochemistryGolgi ApparatusGestational AgeBiologyMonoclonal antibodyPathology and Forensic MedicineEpitopeschemistry.chemical_compoundNeurofilament ProteinsmedicineHumansParaformaldehydeNeuronsPyramidal CellsfungiInfant NewbornAntibodies MonoclonalBrainAbortion InducedDendritesCell BiologyImmunohistochemistryAxonsmedicine.anatomical_structurenervous systemchemistryImmunohistochemistryNeuronNeuroscienceImmunostainingCell and Tissue Research
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Alterations in membrane and firing properties of layer 2/3 pyramidal neurons following focal laser lesions in rat visual cortex.

2013

Focal cortical injuries are well known to cause changes in function and excitability of the surviving cortical areas but the cellular correlates of these physiological alterations are not fully understood. In the present study we employed a well established ex vivo-in vitro model of focal laser lesions in the rat visual cortex and we studied membrane and firing properties of the surviving layer 2/3 pyramidal neurons. Patch-clamp recordings, performed in the first week post-injury, revealed an increased input resistance, a depolarized spike threshold as well as alterations in the firing pattern of neurons in the cortex ipsilateral to the lesion. Notably, the reported lesion-induced alteratio…

Patch-Clamp TechniquesAction PotentialsGABAB receptorBiologyIn Vitro TechniquesSynaptic TransmissionGlutamatergicchemistry.chemical_compoundCortex (anatomy)Biological neural networkmedicineDNQXAnimalsRats Long-EvansVisual CortexMembrane potentialNeuronsGABAA receptorGeneral NeuroscienceLasersPyramidal CellsCell MembraneElectrophysiological PhenomenaRatsVisual cortexmedicine.anatomical_structurechemistryData Interpretation StatisticalSynapsesNeuroscienceNeuroscience
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