Search results for "Synaptic plasticity"

showing 10 items of 132 documents

Oxidative Stress in Neurodegenerative Diseases: From a Mitochondrial Point of View

2019

Age is the main risk factor for a number of human diseases, including neurodegenerative disorders such as Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis, which increasing numbers of elderly individuals suffer. These pathological conditions are characterized by progressive loss of neuron cells, compromised motor or cognitive functions, and accumulation of abnormally aggregated proteins. Mitochondrial dysfunction is one of the main features of the aging process, particularly in organs requiring a high-energy source such as the heart, muscles, brain, or liver. Neurons rely almost exclusively on the mitochondria, which produce the energy required for most of the cel…

AgingAntioxidantMitochondrial Diseasesmedicine.medical_treatmentneurodegeneration oxidative stress mitochondiaDiseaseReview ArticleMitochondrionBiologymedicine.disease_causeBiochemistryAntioxidantsAlzheimer DiseasemedicineHumansAmyotrophic lateral sclerosislcsh:QH573-671lcsh:CytologyNeurodegenerationParkinson DiseaseCell BiologyGeneral Medicinemedicine.diseaseMitochondriaOxidative Stressmedicine.anatomical_structureSynaptic plasticityNeuronNeuroscienceOxidative stress
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A53T-Alpha-Synuclein Overexpression Impairs Dopamine Signaling and Striatal Synaptic Plasticity in Old Mice

2010

BACKGROUND: Parkinson's disease (PD), the second most frequent neurodegenerative disorder at old age, can be caused by elevated expression or the A53T missense mutation of the presynaptic protein alpha-synuclein (SNCA). PD is characterized pathologically by the preferential vulnerability of the dopaminergic nigrostriatal projection neurons. METHODOLOGY/PRINCIPAL FINDINGS: Here, we used two mouse lines overexpressing human A53T-SNCA and studied striatal dysfunction in the absence of neurodegeneration to understand early disease mechanisms. To characterize the progression, we employed young adult as well as old mice. Analysis of striatal neurotransmitter content demonstrated that dopamine (DA…

AgingDopaminelcsh:MedicineMicechemistry.chemical_compoundHomer Scaffolding ProteinsReceptor Cannabinoid CB1lcsh:ScienceLong-term depressionNeurotransmitterChromatography High Pressure LiquidIn Situ Hybridization FluorescenceOligonucleotide Array Sequence AnalysisMice KnockoutNeuronal PlasticityMultidisciplinaryReverse Transcriptase Polymerase Chain ReactionDopaminergicNeurodegenerationGenetics and Genomics/Gene ExpressionElectrophysiologyalpha-SynucleinResearch ArticleRadioimmunoprecipitation Assaymedicine.medical_specialtyNeuronal Calcium-Sensor ProteinsHOMER1Substantia nigraNeurotransmissionBiologyNeurological DisordersInternal medicinemedicineAnimalsHumansddc:610Cyclic Nucleotide Phosphodiesterases Type 7Activating Transcription Factor 2lcsh:RNeuropeptidesmedicine.diseaseMolecular biologyCorpus StriatumMice Mutant StrainsEndocrinologyGenetics and Genomics/Disease ModelschemistrySynaptic plasticitylcsh:QCarrier ProteinsPLoS ONE
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ADAM-10 over-expression increases cortical synaptogenesis.

2006

Cortical cholinergic, glutamatergic and GABAergic terminals become upregulated during early stages of the transgenic amyloid pathology. Abundant evidence suggests that sAPP alpha, the product of the non-amyloidogenic alpha-secretase pathway, is neurotrophic both in vitro and when exogenously applied in vivo. The disintegrin metalloprotease ADAM-10 has been shown to have alpha-secretase activity in vivo. To determine whether sAPP alpha has an endogenous biological influence on cortical presynaptic boutons in vivo, we quantified cortical cholinergic, glutamatergic and GABAergic presynaptic bouton densities in either ADAM-10 moderate expressing (ADAM-10 mo) transgenic mice, which moderately ov…

Agingmedicine.medical_specialtySynaptogenesisPresynaptic TerminalsAlpha (ethology)Mice TransgenicBiologyReceptors Metabotropic GlutamateGlutamatergicADAM10 ProteinMiceReceptors GABAInternal medicinemedicineAnimalsHumansReceptors CholinergicCerebral CortexGeneral NeuroscienceGene Expression Regulation DevelopmentalMembrane Proteinscarbohydrates (lipids)ADAM Proteinsmedicine.anatomical_structureEndocrinologyCerebral cortexSynaptic plasticitySynapsesbiology.proteinGABAergicCholinergicCattleNeurology (clinical)Geriatrics and GerontologyAmyloid Precursor Protein SecretasesDevelopmental BiologyNeurotrophinNeurobiology of aging
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Stressor-related impairment of synaptic transmission in hippocampal slices from α-synuclein knockout mice

2004

The role of alpha-synuclein (alpha-Syn) has recently received considerable attention because it seems to play a role in Parkinson's disease (PD). Missense mutations in the alpha-Syn gene were found in autosomal dominant PD and alpha-Syn was shown to be a major constituent of protein aggregates in sporadic PD and other synucleinopathies. Under normal conditions, alpha-Syn protein is found exclusively in synaptic terminals. However, the potential participation of alpha-synuclein in maintaining and regulating synaptic efficacy is unknown. We have investigated the excitatory synaptic modulation of alpha-synuclein in CA1 pyramidal neurons, using the in vitro hippocampal slice technique. The 4-am…

Alpha-synucleinanimal diseasesGeneral NeuroscienceHippocampusNeurotransmissionBiologynervous system diseaseschemistry.chemical_compoundSynaptic fatiguenervous systemchemistrySynaptic augmentationSynaptic plasticityKnockout mouseExcitatory postsynaptic potentialNeuroscienceEuropean Journal of Neuroscience
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Targeted rescue of synaptic plasticity improves cognitive decline after severe systemic inflammation

2021

AbstractSepsis-associated encephalopathy (SAE) is a frequent complication in patients with severe systemic infection resulting in acute brain dysfunction and incapacitating long-term sequelae. SAE includes delirium, premature death, post-traumatic stress disorder, and major long-term cognitive impairment. The underlying pathophysiology of SAE is largely unresolved and specific treatment options are missing. We induced the peritoneal contamination and infection (PCI) sepsis model in 769 mice and compared these with 259 control mice. We found that experimental sepsis causes synaptic pathology in the brain characterized by severely disordered synaptic plasticity with reduced long-term potentia…

Arc (protein)Synaptic scalingDendritic spinebusiness.industrySynaptic plasticityExcitatory postsynaptic potentialMedicineHippocampusLong-term potentiationSynaptic signalingbusinessNeuroscience
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Minireview: pH and synaptic transmission

2013

AbstractAs a general rule a rise in pH increases neuronal activity, whereas it is dampened by a fall of pH. Neuronal activity per se also challenges pH homeostasis by the increase of metabolic acid equivalents. Moreover, the negative membrane potential of neurons promotes the intracellular accumulation of protons. Synaptic key players such as glutamate receptors or voltage-gated calcium channels show strong pH dependence and effects of pH gradients on synaptic processes are well known. However, the processes and mechanisms that allow controlling the pH in synaptic structures and how these mechanisms contribute to normal synaptic function are only beginning to be resolved.

BiophysicsNeurotransmissionBiochemistryMouse modelGABAStructural BiologySynaptic augmentationGeneticsAnimalsHumansPremovement neuronal activitySynaptic transmissionMolecular BiologyNeuronal excitabilityCarbonic AnhydrasesAcid-Base EquilibriumMembrane potentialCarbonic anhydraseVoltage-dependent calcium channelChemistryGlutamate receptorCell BiologyBicarbonatesSynaptic fatigueBiochemistrypH regulationSynapsesSynaptic plasticityBiophysicsIon transporterFEBS Letters
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Stably BDNF-GFP expressing embryonic stem cells exhibit a BDNF release-dependent enhancement of neuronal differentiation

2013

Brain-derived neurotrophic factor (BDNF) is known to be a crucial regulator of neuronal survival and synaptic plasticity in the mammalian brain. Furthermore, BDNF positively influences differentiation of embryonic neural precursors as well as of neural stem cells from adult neurogenic niches. To study the impact of cell-released BDNF on neural differentiation of embryonic stem cells (ESCs), which represent an attractive source for cell transplantation studies, we have generated BDNF-GFP overexpressing mouse ESC clones by knock-in technology. After neural differentiation in vitro, we observed that BDNF-GFP overexpressing ESC clones gave rise to an increased number of neurons as compared to c…

Brain-derived neurotrophic factorCell BiologyAnatomyBiologyEmbryonic stem cellNeural stem cellCell biologyGreen fluorescent proteinTransplantationnervous systemNeurotrophic factorsembryonic structuresSynaptic plasticityGABAergicJournal of Cell Science
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Postsynaptic Secretion of BDNF and NT-3 from Hippocampal Neurons Depends on Calcium–Calmodulin Kinase II Signaling and Proceeds via Delayed Fusion Po…

2007

The mammalian neurotrophins (NTs) NGF, BDNF, NT-3, and NT-4 constitute a family of secreted neuronal growth factors. In addition, NTs are implicated in several forms of activity-dependent synaptic plasticity. Although synaptic secretion of NTs has been described, the intracellular signaling cascades that regulate synaptic secretion of NTs are far from being understood. Analysis of NT secretion at the subcellular level is thus required to resolve the role of presynaptic and postsynaptic NT secretion for synaptic plasticity. Here, we transfected cultures of dissociated rat hippocampal neurons with green fluorescent protein-tagged versions of BDNF and NT-3, respectively, and identified NT vesi…

Calcium Channels L-TypeBiologyNeurotransmissionInhibitory postsynaptic potentialHippocampusReceptors N-Methyl-D-AspartateSynaptic TransmissionExocytosisNeurotrophin 3Postsynaptic potentialCa2+/calmodulin-dependent protein kinaseAnimalsCalcium SignalingNeuronsBrain-Derived Neurotrophic FactorGeneral NeuroscienceRyanodine Receptor Calcium Release ChannelLong-term potentiationArticlesCyclic AMP-Dependent Protein KinasesRatsCell biologynervous systemBiochemistryTrk receptorCalcium-Calmodulin-Dependent Protein KinasesSynapsesSynaptic plasticityThapsigarginCalcium-Calmodulin-Dependent Protein Kinase Type 2Postsynaptic densityThe Journal of Neuroscience
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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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Neural inflammation alters synaptic plasticity probed by 10 Hz repetitive magnetic stimulation

2020

ABSTRACTSystemic inflammation is associated with alterations in complex brain functions such as learning and memory. However, diagnostic approaches to functionally assess and quantify inflammation-associated alterations in synaptic plasticity are not well-established. In previous work, we demonstrated that bacterial lipopolysaccharide (LPS)-induced systemic inflammation alters the ability of hippocampal neurons to express synaptic plasticity, i.e., the long-term potentiation (LTP) of excitatory neurotransmission. Here, we tested whether synaptic plasticity induced by repetitive magnetic stimulation (rMS), a non-invasive brain stimulation technique used in clinical practice, is affected by L…

ChemistryBrain stimulationSynaptic plasticityExcitatory postsynaptic potentialStimulationTumor necrosis factor alphaLong-term potentiationNeurotransmissionHippocampal formationNeuroscience
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