Search results for "Excitatory Amino Acid Antagonists"

showing 10 items of 55 documents

Intracellular Na+ concentration influences short-term plasticity of glutamate transporter-mediated currents in neocortical astrocytes.

2012

Fast synaptic transmission requires a rapid clearance of the released neurotransmitter from the extracellular space. Glial glutamate transporters (excitatory amino acid transporters, EAATs) strongly contribute to glutamate removal. In this work, we investigated the paired-pulse plasticity of synaptically activated, glutamate transporter-mediated currents (STCs) in cortical layer 2/3 astrocytes. STCs were elicited by local electrical stimulation in layer 4 in the presence of ionotropic glutamate (AMPA and NMDA), GABAA, and GABAB receptor antagonists. In experiments with low [Na+]i (5 mM) intrapipette solution, STCs elicited by paired-pulse stimulation demonstrated paired-pulse facilitation (…

Intracellular FluidPatch-Clamp TechniquesAmino Acid Transport System X-AGBiophysicsNipecotic AcidsAction PotentialsNeocortexAMPA receptorTetrodotoxinBiologyGABAB receptorAnisolesIn Vitro TechniquesSynaptic TransmissionGABA AntagonistsCellular and Molecular NeuroscienceMiceCadmium ChlorideEthers CyclicOximesmedicineGABA transporterAnimalsgamma-Aminobutyric AcidBenzofuransAspartic AcidNeuronal PlasticityGABAA receptorRhodaminesSodiumGlutamate receptorCalcium Channel BlockersElectric StimulationMice Inbred C57BLmedicine.anatomical_structureNeurologyAnimals NewbornAstrocytesExcitatory postsynaptic potentialBiophysicsbiology.proteinNMDA receptorNeuroscienceExcitatory Amino Acid AntagonistsAstrocyteSodium Channel BlockersGlia
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Modulation of NMDA receptor function by cyclic AMP in cerebellar neurones in culture

2004

The signal transduction pathways involved in NMDA receptor modulation by other receptors remain unclear. cAMP could be involved in this modulation. The aim of this work was to analyse the contribution of cAMP to NMDA receptor modulation in cerebellar neurones in culture. Forskolin increases cAMP and results in increased intracellular calcium and cGMP that are prevented by blocking NMDA receptors. Similar effects were induced by two cAMP analogues, indicating that cAMP leads to NMDA receptor activation. It has been reported that phosphorylation of Ser897 of the NR1 subunit of NMDA receptors by cAMP-dependent protein kinase (PKA) activates the receptors. Forskolin increases Ser897 phosphoryla…

Intracellular Fluidmedicine.medical_specialty8-Bromo Cyclic Adenosine MonophosphateBiologyReceptors N-Methyl-D-AspartateBiochemistryCellular and Molecular Neurosciencechemistry.chemical_compoundCerebellumInternal medicineCyclic AMPmedicineAnimalsCyclic adenosine monophosphateNerve Growth FactorsEnzyme InhibitorsPhosphorylationRats WistarProtein kinase AReceptorLong-term depressionCyclic GMPCells CulturedNeuronsNeurotransmitter AgentsForskolinColforsinNeuropeptidesCyclic AMP-Dependent Protein KinasesRatsPituitary adenylate cyclase-activating peptideEndocrinologynervous systemchemistryPituitary Adenylate Cyclase-Activating PolypeptideNMDA receptorCalciumSignal transductionExcitatory Amino Acid AntagonistsSignal TransductionJournal of Neurochemistry
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Activation of metabotropic glutamate receptors induces propagating network oscillations in the intact cerebral cortex of the newborn mouse.

2006

Activation of metabotropic glutamate receptors (mGluRs) with (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid (ACPD) elicited in the frontal or occipital pole of the intact cerebral cortex preparation of the newborn mouse (P0-P3) a transient oscillatory field potential activity in the frequency range of 11-14Hz. These oscillations propagated over the whole cortical hemisphere and were blocked by tetrodotoxin, indicating that action potentials are required for the generation of this activity. Blockade of GABA-A receptors with gabazine did not influence the ACPD-induced network activity, but the glycine antagonist strychnine caused a significant decrease in the frequency, amplitude and durat…

Kainate receptorCholinergic AgonistsReceptors Metabotropic GlutamateCellular and Molecular Neurosciencechemistry.chemical_compoundMiceKynurenic acidmedicineAnimalsLong-term depressionPharmacologyCerebral CortexDose-Response Relationship DrugDioxolanesEnzyme ActivationMice Inbred C57BLchemistryAnimals NewbornMetabotropic glutamate receptorPurinesCNQXGabazineACPDNMDA receptorCarbacholNerve NetNeuroscienceExcitatory Amino Acid Antagonistsmedicine.drugNeuropharmacology
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Subventricular zone neural progenitors protect striatal neurons from glutamatergic excitotoxicity.

2012

The functional significance of adult neural stem and progenitor cells in hippocampal-dependent learning and memory has been well documented. Although adult neural stem and progenitor cells in the subventricular zone are known to migrate to, maintain and reorganize the olfactory bulb, it is less clear whether they are functionally required for other processes. Using a conditional transgenic mouse model, selective ablation of adult neural stem and progenitor cells in the subventricular zone induced a dramatic increase in morbidity and mortality of central nervous system disorders characterized by excitotoxicity-induced cell death accompanied by reactive inflammation, such as 4-aminopyridine-i…

LipopolysaccharidesPolyunsaturated AlkamidesSubventricular zoneGlutamic AcidMice TransgenicArachidonic AcidsBiologyAmidohydrolasesGlutamatergicMiceNeural Stem CellsLateral VentriclesmedicineAnimalsDronabinolProgenitor cell4-Aminopyridineneurogenesis; ischaemia; neural stem cells; excitotoxicity; endocannabinoidsGanciclovirEpilepsyStem CellsNeurogenesisExcitatory Postsynaptic PotentialsNeural stem cellCorpus StriatumNeuroepithelial cellMice Inbred C57BLStrokeneurogenesisDisease Models Animalmedicine.anatomical_structureNeuroprotective AgentsBenzamidesSettore MED/26 - NeurologiaNeurology (clinical)ischaemiaCarbamatesStem cellNeuroscienceexcitotoxicityExcitatory Amino Acid AntagonistsAdult stem cellEndocannabinoidsBrain : a journal of neurology
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MK801 blocks hypoxic blood-brain-barrier disruption and leukocyte adhesion.

2008

The aim of the present study was to examine the signaling pathways of hypoxia followed by reoxygenation (H/R)-induced disruption of the blood-brain-barrier (BBB) in a co-culture of astrocytes and brain endothelial cells (BEC) in vitro. We analyzed the possible stabilizing effect of MK801, a highly selective N-methyl-d-aspartate receptor (NMDAR) antagonist, on BBB integrity. Levels of reactive oxygen species (ROS), glutamate (Glut) release and monocyte adhesion were measured under normoxia and H/R. BBB integrity was monitored measuring the trans-endothelial electrical resistance (TEER). TEER values dropped under H/R conditions which was abolished by MK801. Glut release from astrocytes, but n…

Macrocyclic CompoundsSwineGlutamic AcidBiologyBlood–brain barrierchemistry.chemical_compoundmedicineExtracellularCell AdhesionElectric ImpedanceLeukocytesAnimalsEnzyme InhibitorsOxazolesCells Culturedchemistry.chemical_classificationReactive oxygen speciesRyanodine receptorRyanodineGeneral NeuroscienceEndoplasmic reticulumGlutamate receptorAcetophenonesBrainEndothelial CellsCell HypoxiaCoculture TechniquesCell biologyOxygenmedicine.anatomical_structurechemistryBlood-Brain BarrierAstrocytesApocyninCalciumNAD+ kinaseDizocilpine MaleateReactive Oxygen SpeciesExcitatory Amino Acid AntagonistsNeuroscience letters
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Temporally precise control of single-neuron spiking by juxtacellular nanostimulation

2017

Temporal patterns of action potentials influence a variety of activity-dependent intra- and intercellular processes and play an important role in theories of neural coding. Elucidating the mechanisms underlying these phenomena requires imposing spike trains with precisely defined patterns, but this has been challenging due to the limitations of existing stimulation techniques. Here we present a new nanostimulation method providing control over the action potential output of individual cortical neurons. Spikes are elicited through the juxtacellular application of short-duration fluctuating currents (“kurzpulses”), allowing for the sub-millisecond precise and reproducible induction of arbitr…

Male0301 basic medicine2-amino-5-phosphopentanoic acidPatch-Clamp TechniquesTime FactorsPhysiologyComputer scienceAction Potentialsgenetics [Luminescent Proteins]pharmacology [Valine]metabolism [Cytoskeletal Proteins]Mice0302 clinical medicineCortex (anatomy)physiology [Action Potentials]genetics [Nerve Tissue Proteins]6-Cyano-7-nitroquinoxaline-23-dioneNeuronsGeneral Neurosciencepharmacology [Excitatory Amino Acid Antagonists]Valinephysiology [Neurons]medicine.anatomical_structurepharmacology [6-Cyano-7-nitroquinoxaline-23-dione]FemaleSpike (software development)Neuroinformaticsgenetics [Synapsins]Models NeurologicalBiophysicsMice TransgenicNerve Tissue ProteinsOptogenetics03 medical and health sciencesmedicinedrug effects [Neurons]Animalsmetabolism [Synapsins]ddc:610metabolism [Luminescent Proteins]activity regulated cytoskeletal-associated proteingenetics [Cytoskeletal Proteins]analogs & derivatives [Valine]metabolism [Nerve Tissue Proteins]drug effects [Action Potentials]Somatosensory CortexSynapsinsElectric StimulationOptogeneticsCytoskeletal ProteinsLuminescent Proteins030104 developmental biologynervous systemInnovative Methodologycytology [Somatosensory Cortex]NeuronWhole cellExcitatory Amino Acid AntagonistsNeuroscience030217 neurology & neurosurgeryJournal of Neurophysiology
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Mild systemic inflammation and moderate hypoxia transiently alter neuronal excitability in mouse somatosensory cortex

2016

During the perinatal period, the brain is highly vulnerable to hypoxia and inflammation, which often cause white matter injury and long-term neuronal dysfunction such as motor and cognitive deficits or epileptic seizures. We studied the effects of moderate hypoxia (HYPO), mild systemic inflammation (INFL), or the combination of both (HYPO + INFL) in mouse somatosensory cortex induced during the first postnatal week on network activity and compared it to activity in SHAM control animals. By performing in vitro electrophysiological recordings with multi-electrode arrays from slices prepared directly after injury (P8–10), one week after injury (P13–16), or in young adults (P28–30), we investig…

Male0301 basic medicineAction PotentialsKainate receptorStimulationPotassium ChlorideMicechemistry.chemical_compound0302 clinical medicineHypoxia6-Cyano-7-nitroquinoxaline-23-dioneNeuronsAge FactorsInterleukin-1βElectrophysiologyEpileptiform activityNeurologyAnesthesiaCNQXNMDA receptorFemalemedicine.symptommedicine.drugmedicine.medical_specialtyAMPA receptorIn Vitro TechniquesBiologyBicucullineMulti-electrode arrayArticlelcsh:RC321-57103 medical and health sciencesInternal medicinemedicineAnimalsGABA-A Receptor Antagonistslcsh:Neurosciences. Biological psychiatry. NeuropsychiatryInflammationSystemic inflammationSomatosensory CortexHypoxia (medical)BicucullineBarrel cortexMice Inbred C57BLDisease Models Animal030104 developmental biologyEndocrinology2-Amino-5-phosphonovalerateGene Expression Regulationchemistrynervous systemExploratory BehaviorExcitatory Amino Acid Antagonists030217 neurology & neurosurgeryNeurobiology of Disease
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Phencyclidine-induced disruption of oscillatory activity in prefrontal cortex: Effects of antipsychotic drugs and receptor ligands

2016

The non-competitive NMDA receptor (NMDA-R) antagonist phencyclidine (PCP) markedly disrupts thalamocortical activity, increasing excitatory neuron discharge and reducing low frequency oscillations (LFO, <4Hz) that temporarily group neuronal discharge. These actions are mainly driven by PCP interaction with NMDA-R in GABAergic neurons of the thalamic reticular nucleus and likely underlie PCP psychotomimetic activity. Here we report that classical (haloperidol, chlorpromazine, perphenazine) and atypical (clozapine, olanzapine, quetiapine, risperidone, ziprasidone, aripripazole) antipsychotic drugs - but not the antidepressant citalopram - countered PCP-evoked fall of LFO in the medial prefron…

Male0301 basic medicineOscillationsmedicine.drug_classDopamine AgentsAtypical antipsychoticPhencyclidineKainate receptorPharmacologyNeurotransmissionPrefrontal cortex03 medical and health scienceschemistry.chemical_compoundSerotonin Agents0302 clinical medicineHistamine AgentsmedicineAnimalsPharmacology (medical)NMDA receptor antagonistsAntipsychotic drugsRats WistarChlorpromazineEvoked PotentialsPhencyclidineBiological PsychiatryPharmacologyRacloprideAnalysis of VarianceDose-Response Relationship DrugFourier AnalysisChemistryElectroencephalographyPsychotomimeticRatsPsychiatry and Mental health030104 developmental biologyNeurologynervous systemSchizophreniaNBQXNeurology (clinical)Excitatory Amino Acid AntagonistsNeuroscience030217 neurology & neurosurgeryAntipsychotic Agentsmedicine.drug
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PSA-NCAM expression in the piriform cortex of the adult rat. Modulation by NMDA receptor antagonist administration.

2002

Administration of NMDA receptor antagonists upregulates the expression of the polysialylated form of the neural cell adhesion molecule (PSA-NCAM) in the adult hippocampus. Since the piriform cortex is also populated by PSA-NCAM immunoreactive neurons during adulthood, we sought to characterize them in detail and to test whether NMDA receptor antagonists also modulate PSA-NCAM in this cortical region. PSA-NCAM immunoreactivity is located mainly in layer II, where many neurogliaform and some pyramidal-semilunar transitional neurons are labeled. Many large neurons in layer III and endopiriform nucleus also express PSA-NCAM. Interestingly, some small labeled cells resembling migratory neuroblas…

MaleDoublecortin ProteinSynaptogenesisHippocampusNeural Cell Adhesion Molecule L1Receptors N-Methyl-D-AspartateRats Sprague-DawleyNeuroblastCell MovementPiriform cortexmedicineAnimalsMolecular BiologyNeural Cell Adhesion MoleculesNeuronsbiologyGeneral NeuroscienceOlfactory PathwaysDoublecortinRatsmedicine.anatomical_structurenervous systembiology.proteinSialic AcidsNeural cell adhesion moleculeNeurology (clinical)NeuNNeuroscienceNucleusExcitatory Amino Acid AntagonistsInjections IntraperitonealDevelopmental BiologyBrain research
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Role of AMPA glutamate receptors in the conditioned rewarding effects of MDMA in mice

2018

Abstract Currently, there is not an effective treatment for 3,4-methylenedioxymethamphetamine (MDMA) dependence but pharmacotherapies targeting glutamate neurotransmission are a promising strategy. Previously, we showed that blockade of glutamate NMDA and AMPA receptors impairs the conditioned rewarding effects of MDMA and cocaine, respectively. In this study we evaluated the role of AMPA receptors in the rewarding effects of MDMA in mice using the conditioned place preference (CPP) paradigm. Mice were conditioned with MDMA (1.25 mg/kg) 60 min after the treatment with saline or different doses (0.25, 1 and 5 mg/kg) of the AMPA/kainate receptor antagonist, 6-cyano-7-nitroquinoxaline-2,3-dion…

MaleHallucinogenMDMAmiceN-Methyl-34-methylenedioxyamphetamineAmphetamine-Related DisordersSpatial BehaviorKainate receptorAMPA receptorPharmacologyMice03 medical and health sciencesBehavioral Neurosciencechemistry.chemical_compound0302 clinical medicineRewardConditioning Psychologicalmental disordersmedicineAnimalsReceptors AMPAAMPA receptorsreward6-Cyano-7-nitroquinoxaline-23-dioneDose-Response Relationship Drugbusiness.industryGlutamate receptorMDMACNQXconditioned place preferenceConditioned place preference030227 psychiatrynervous systemchemistryHallucinogensCNQXNMDA receptorbusinessExcitatory Amino Acid Antagonistspsychological phenomena and processes030217 neurology & neurosurgerymedicine.drugBehavioural Brain Research
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