Search results for "LONG-TERM POTENTIATION"

showing 10 items of 101 documents

Ebselen prevents chronic alcohol-induced rat hippocampal stress and functional impairment

2007

Background: Most of the previously published data suggest a role for oxidative or nitrosative stress in ethanol-induced nervous system damage. Moreover, ethanol is able to impair learning abilities in adult mammalian brain, a process suggested to be directly related to hippocampal neurogenesis. Ebselen, a synthetic compound with antioxidant properties, is able to prevent ethanol-induced impairment of neurogenesis in adult rats. The aim of the present work was to further demonstrate the ability of ebselen to prevent biochemical alterations, and preserve long-term potentiation (LTP) and learning abilities, in the hippocampus of chronic alcoholic adult rats. Methods: Biochemical markers of oxi…

AzolesMalemedicine.medical_specialtyAlcohol DrinkinghippocampusoxidationLong-Term PotentiationSpatial BehaviorMedicine (miscellaneous)Morris water navigation taskIsoindolesHippocampal formationToxicologymedicine.disease_causeHippocampusAntioxidantsRats Sprague-Dawleychemistry.chemical_compoundOrganoselenium CompoundsInternal medicinemedicineAnimalsMaze Learninglong-term potentiationlearningEbselenNeurogenesisLong-term potentiationGlutathioneMalondialdehydeGlutathioneRatsOxidative StressPsychiatry and Mental healthEndocrinologychemistryBiochemistryethanolOxidative stress
researchProduct

Heme oxygenase-1 induction by nitric oxide in RAW 264.7 macrophages is upregulated by a cyclo-oxygenase-2 inhibitor.

2001

Unstimulated RAW 264.7 macrophages express negligible heme oxygenase-1 (HO-1) protein but incubation with the nitric oxide (NO) donor spermine nonoate (SPNO) induced HO-1 and weakly cyclo-oxygenase-2 (COX-2) protein. This effect was potentiated by coincubation with the COX-2 selective inhibitor, SC58125. Cells incubated with SPNO showed a strong increase in HO-1 mRNA levels after 4 h with a significant potentiation in the presence of SC58125, which did not modify HO-1 mRNA stability. The induction of HO-1 by NO and its potentiation by anti-inflammatory agents may play a role in inflammatory and immune responses.

BiophysicsSpermineNitric OxideBiochemistryNitric oxideCell Linechemistry.chemical_compoundMiceDownregulation and upregulationMacrophageAnimalsCyclooxygenase InhibitorsRNA MessengerMolecular BiologyHemeCyclooxygenase 2 InhibitorsMacrophagesMembrane ProteinsLong-term potentiationDrug SynergismMolecular biologyUp-RegulationHeme oxygenaseIsoenzymeschemistryBiochemistryCell cultureCyclooxygenase 2Prostaglandin-Endoperoxide SynthasesHeme Oxygenase (Decyclizing)PyrazolesNitrogen OxidesSpermineHeme Oxygenase-1Biochimica et biophysica acta
researchProduct

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
researchProduct

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
researchProduct

Neurotrophin secretion: current facts and future prospects

2003

The proteins of the mammalian neurotrophin family (nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3) and neurotrophin-4/5 (NT-4/5)) were originally identified as neuronal survival factors. During the last decade, evidence has accumulated implicating them (especially BDNF) in addition in the regulation of synaptic transmission and synaptogenesis in the CNS. However, a detailed understanding of the secretion of neurotrophins from neurons is required to delineate their role in regulating synaptic function. Some crucial questions that need to be addressed include the sites of neurotrophin secretion (i.e. axonal versus dendritic; synaptic versus extrasyna…

Central Nervous SystemNeuronsNeuronal PlasticityArc (protein)biologyCell SurvivalGeneral NeuroscienceSynaptogenesisLong-term potentiationAMPA receptorNeurotransmissionCell Linenervous systemNeurotrophic factorsTrk receptorbiology.proteinAnimalsHumansNerve Growth FactorsPeptidesNeuroscienceForecastingNeurotrophinProgress in Neurobiology
researchProduct

Purkinje cell loss and motor coordination defects in profilin1 mutant mice.

2012

Profilin1 is an actin monomer-binding protein, essential for cytoskeletal dynamics. Based on its broad expression in the brain and the localization at excitatory synapses (hippocampal CA3-CA1 synapse, cerebellar parallel fiber (PF)-Purkinje cell (PC) synapse), an important role for profilin1 in brain development and synapse physiology has been postulated. We recently showed normal physiology of hippocampal CA3-CA1 synapses in the absence of profilin1, but impaired glial cell binding and radial migration of cerebellar granule neurons (CGNs). Consequently, brain-specific inactivation of profilin1 by exploiting conditional mutants and Nestin-mediated cre expression resulted in a cerebellar hyp…

CerebellumPatch-Clamp TechniquesPurkinje cellBiophysicsAction PotentialsParallel fiberMice TransgenicNerve Tissue ProteinsBiologyHippocampal formationIn Vitro TechniquesMotor ActivitySynapseNestinMiceProfilinsPurkinje CellsIntermediate Filament ProteinsmedicineAnimalsGeneral NeuroscienceAge FactorsBrainGene Expression Regulation DevelopmentalLong-term potentiationElectric StimulationDisease Models Animalmedicine.anatomical_structurenervous systemCytoarchitectureAnimals NewbornCerebellar cortexMutationDisease ProgressionPsychomotor DisordersNeuroscienceNeuroscience
researchProduct

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
researchProduct

Long-Term Potentiation in the Recurrent Inhibitory Circuit of the Dentate Gyrus

1988

The question of whether long-term potentiation occurs in the inhibitory circuits of the hippocampus remains controversial. Buszaki and Eidelberg (1982), recording extracellularly from putative interneurones (basket cells) in the dentate gyrus and area CAl of the anaesthetized rat, found a prolonged increase in probability of cell firing to afferent stimulation after high-frequency stimulation of Schaffer-commissural fibres, and concluded that LTP occurs at excitatory feedforward synapses onto interneurones. Similarly, Kairis et al (1987) have presented field potential evidence for LTP in feedforward synapses onto inhibitory neurones in the dentate gyrus of the anaesthetized rat. In the hipp…

Chemistrymusculoskeletal neural and ocular physiologyDentate gyrusHippocampusLong-term potentiationPerforant pathInhibitory postsynaptic potentialGranule cellmedicine.anatomical_structurenervous systemBasket cellmedicineExcitatory postsynaptic potentialNeuroscience
researchProduct

Neuromuscular junction disassembly and muscle fatigue in mice lacking neurotrophin-4

2001

Neurotrophin-4 (NT-4) is produced by slow muscle fibers in an activity-dependent manner and promotes growth and remodeling of adult motorneuron innervation. However, both muscle fibers and motor neurons express NT-4 receptors, suggesting bidirectional NT-4 signaling at the neuromuscular junction. Mice lacking NT-4 displayed enlarged and fragmented neuromuscular junctions with disassembled postsynaptic acetylcholine receptor (AChR) clusters, reduced AChR binding, and acetylcholinesterase activity. Electromyographic responses, posttetanic potentiation, and action potential amplitude were also significantly reduced in muscle fibers from NT-4 knock-out mice. Slow-twitch soleus muscles from thes…

End-plate potentialNeuromuscular JunctionElectromyographyBiologyNeuromuscular junctionCellular and Molecular NeuroscienceMicePostsynaptic potentialmedicineAnimalsReceptors CholinergicNerve Growth FactorsMuscle SkeletalMolecular BiologyAcetylcholine receptorMice KnockoutMotor Neuronsmedicine.diagnostic_testMuscle fatigueElectromyographyAge FactorsLong-term potentiationneuromuscular junction; neurotrophin-4; synaptic transmissionCell Biologymedicine.anatomical_structureMuscle Fibers Slow-TwitchMuscle FatigueAcetylcholinesteraseTetanic stimulationNeuroscienceMuscle Contraction
researchProduct

Prenatal low-level exposure to CO alters postnatal development of hippocampal nitric oxide synthase and haem-oxygenase activities in rats.

2001

The effects of prenatal CO exposure (150 ppm from days 0 to 20 of pregnancy) on the postnatal development of hippocampal neuronal NO synthase (nNOS) and haem-oxygenase (HO-2) isoform activities in 15-, 30- and 90-d-old rats were investigated. Unlike HO-2, hippocampal nNOS activity increased from postnatal days 15-90 in controls. Prenatal CO produced a long-lasting decrease in either nNOS or HO-2. The results suggest that the altered developmental profile of hippocampal nNOS and HO-2 activities could be involved in cognitive deficits and long-term potentiation dysfunction exhibited by rats prenatally exposed to CO levels resulting in carboxyhaemoglobin (HbCO) levels equivalent to those obser…

Gene isoformmedicine.medical_specialtyNitric Oxide Synthase Type IHippocampal formationHippocampusCarbon monoxide; haem-oxygenase; hippocampus; nitric oxide synthase; prenatal exposure.HemoglobinsPregnancyInternal medicinemedicineAnimalsPharmacology (medical)Rats WistarPharmacologyDevelopmental profilePregnancyCarbon MonoxidebiologyChemistryLong-term potentiationLow level exposuremedicine.diseaseHaem OxygenaseRatsNitric oxide synthaseIsoenzymesPsychiatry and Mental healthEndocrinologyPrenatal Exposure Delayed EffectsHeme Oxygenase (Decyclizing)biology.proteinFemaleNitric Oxide SynthaseThe international journal of neuropsychopharmacology
researchProduct