Search results for "Pyramidal cell"

showing 10 items of 51 documents

A modeling study suggesting how a reduction in the context-dependent input on CA1 pyramidal neurons could generate schizophrenic behavior.

2011

The neural mechanisms underlying schizophrenic behavior are unknown and very difficult to investigate experimentally, although a few experimental and modeling studies suggested possible causes for some of the typical psychotic symptoms related to this disease. The brain region most involved in these processes seems to be the hippocampus, because of its critical role in establishing memories for objects or events in the context in which they occur. In particular, a hypofunction of the N-methyl-D-aspartate (NMDA) component of the synaptic input on the distal dendrites of CA1 pyramidal neurons has been suggested to play an important role for the emergence of schizophrenic behavior. Modeling st…

Computer scienceCognitive Neurosciencemedia_common.quotation_subjectSchizophrenia Realistic model CA1 Hippocampus Object recognition Synaptic integrationCentral nervous systemModels NeurologicalCa1 neuronHippocampusHippocampal formationSynapse03 medical and health sciences0302 clinical medicineArtificial IntelligencePerceptionmedicineAnimalsHumansInvariant (mathematics)CA1 Region Hippocampal030304 developmental biologymedia_common0303 health sciencesRecallArtificial neural networkPyramidal NeuronSynaptic integrationPyramidal CellsCognitive neuroscience of visual object recognitionDendritesmedicine.diseasemedicine.anatomical_structurenervous systemSchizophreniaSynapsesSchizophreniaNMDA receptorNeuronNerve NetNeuroscience030217 neurology & neurosurgeryNeural networks : the official journal of the International Neural Network Society
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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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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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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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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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Lack of APP and APLP2 in GABAergic Forebrain Neurons Impairs Synaptic Plasticity and Cognition.

2020

AbstractAmyloid-β precursor protein (APP) is central to the pathogenesis of Alzheimer’s disease, yet its physiological functions remain incompletely understood. Previous studies had indicated important synaptic functions of APP and the closely related homologue APLP2 in excitatory forebrain neurons for spine density, synaptic plasticity, and behavior. Here, we show that APP is also widely expressed in several interneuron subtypes, both in hippocampus and cortex. To address the functional role of APP in inhibitory neurons, we generated mice with a conditional APP/APLP2 double knockout (cDKO) in GABAergic forebrain neurons using DlxCre mice. These DlxCre cDKO mice exhibit cognitive deficits i…

InterneuronCognitive NeuroscienceLong-Term PotentiationSpatial LearningHippocampusAction PotentialsInhibitory postsynaptic potentialHippocampusNesting Behavior03 medical and health sciencesCellular and Molecular NeuroscienceAmyloid beta-Protein PrecursorMice0302 clinical medicineCognitionProsencephalonAmyloid precursor proteinmedicineAnimalsGABAergic NeuronsCA1 Region Hippocampal030304 developmental biologySpatial MemoryMice Knockout0303 health sciencesNeuronal PlasticitybiologyPyramidal CellsExcitatory Postsynaptic PotentialsLong-term potentiationmedicine.anatomical_structurenervous systemInhibitory Postsynaptic PotentialsSynaptic plasticityForebrainExcitatory postsynaptic potentialbiology.proteinNeuroscience030217 neurology & neurosurgeryCerebral cortex (New York, N.Y. : 1991)
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Chronic benzodiazepine treatment decreases spine density in cortical pyramidal neurons.

2015

The adult brain retains a substantial capacity for synaptic reorganization, which includes a wide range of modifications from molecular to structural plasticity. Previous reports have demonstrated that the structural remodeling of excitatory neurons seems to occur in parallel to changes in GABAergic neurotransmission. The function of neuronal inhibitory networks can be modified through GABAA receptors, which have a binding site for benzodiazepines (BZ). Although BZs are among the most prescribed drugs, is not known whether they modify the structure and connectivity of pyramidal neurons. In the present study we wish to elucidate the impact of a chronic treatment of 21 days with diazepam (2mg…

0301 basic medicineCingulate cortexMaleDendritic spineDendritic SpinesPrefrontal CortexMice TransgenicBiologyInhibitory postsynaptic potential03 medical and health sciences0302 clinical medicinePostsynaptic potentialAnimalsGABA-A Receptor AgonistsDiazepamBehavior AnimalDose-Response Relationship DrugGABAA receptorGeneral NeurosciencePyramidal Cellsfood and beveragesLong-term potentiation030104 developmental biologynervous systemExcitatory postsynaptic potentialGABAergicNeuroscience030217 neurology & neurosurgeryNeuroscience letters
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PSA-NCAM expression in the rat medial prefrontal cortex

2005

The rat medial prefrontal cortex, an area considered homologous to the human prefrontal cortex, is a region in which neuronal structural plasticity has been described during adulthood. Some plastic processes such as neurite outgrowth and synaptogenesis are known to be regulated by the polysialylated form of the neural cell adhesion molecule (PSA-NCAM). Since PSA-NCAM is present in regions of the adult CNS which are undergoing structural remodeling, such as the hypothalamus or the hippocampus, we have analyzed the expression of this molecule in the medial prefrontal cortex of adult rats using immunohistochemistry. PSA-NCAM immunoreactivity was found both in cell bodies and in the neuropil of…

MaleNeuropilNeuriteInterneuronAntimetabolitesCell SurvivalSynaptophysinSynaptogenesisPrefrontal CortexHippocampusNeural Cell Adhesion Molecule L1BiologyRats Sprague-DawleyNeuroplasticityNeuropilmedicineAnimalsFluorescent Antibody Technique IndirectPrefrontal cortexNeuronsNeuronal PlasticityGlutamate DecarboxylasePyramidal CellsGeneral NeuroscienceImmunohistochemistryRatsPhenotypemedicine.anatomical_structureBromodeoxyuridinenervous systemSialic AcidsNeural cell adhesion moleculeNeuroscienceNeuroscience
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Optogenetically blocking sharp wave ripple events in sleep does not interfere with the formation of stable spatial representation in the CA1 area of …

2016

During hippocampal sharp wave/ripple (SWR) events, previously occurring, sensory inputdriven neuronal firing patterns are replayed. Such replay is thought to be important for plasticity-related processes and consolidation of memory traces. It has previously been shown that the electrical stimulation-induced disruption of SWR events interferes with learning in rodents in different experimental paradigms. On the other hand, the cognitive map theory posits that the plastic changes of the firing of hippocampal place cells constitute the electrophysiological counterpart of the spatial learning, observable at the behavioral level. Therefore, we tested whether intact SWR events occurring during th…

LightPhysiologylcsh:MedicineHippocampusTetrodesMiceAnimal Cells571 PhysiologyMedicine and Health Scienceslcsh:ScienceNeuronsLight PulsesBrain MappingNeuronal PlasticityPyramidal CellsPhysicsElectromagnetic RadiationBrainLaboratory EquipmentSignal Filteringsharp wave ripple eventesBioassays and Physiological AnalysisOptical EquipmentVacuum ApparatusPhysical SciencesEngineering and TechnologyFemaleCellular TypesAnatomyResearch ArticleGanglion CellsArchaeal ProteinsSpatial LearningEquipmentResearch and Analysis Methodsuni (lepotila)AnimalshippokampusCA1 Region HippocampalLaserslcsh:RCorrectionBiology and Life SciencesNeurophysiological AnalysisCell BiologyBrain WavesMice Inbred C57BLOptogeneticsCellular NeuroscienceSignal ProcessingExploratory Behavior570 Life sciences; biologylcsh:QPhysiological ProcessesSleepNeuroscience
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Dysregulated Expression of Neuregulin-1 by Cortical Pyramidal Neurons Disrupts Synaptic Plasticity

2014

Summary Neuregulin-1 ( NRG1 ) gene variants are associated with increased genetic risk for schizophrenia. It is unclear whether risk haplotypes cause elevated or decreased expression of NRG1 in the brains of schizophrenia patients, given that both findings have been reported from autopsy studies. To study NRG1 functions in vivo, we generated mouse mutants with reduced and elevated NRG1 levels and analyzed the impact on cortical functions. Loss of NRG1 from cortical projection neurons resulted in increased inhibitory neurotransmission, reduced synaptic plasticity, and hypoactivity. Neuronal overexpression of cysteine-rich domain (CRD)-NRG1, the major brain isoform, caused unbalanced excitato…

MaleDendritic SpinesNeuregulin-1Nonsynaptic plasticityGene ExpressionMice TransgenicNeurotransmissionInhibitory postsynaptic potentialSynaptic TransmissionGeneral Biochemistry Genetics and Molecular BiologyCell MovementInterneuronsConditioning Psychologicalmental disordersAnimalsNeuregulin 1lcsh:QH301-705.5CA1 Region HippocampalNeuronal PlasticitybiologyPyramidal CellsAnatomyFearCortex (botany)Synaptic fatiguelcsh:Biology (General)Synaptic plasticitybiology.proteinExcitatory postsynaptic potentialFemaleNerve NetNeuroscience
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