Search results for "N-Methylaspartate"

showing 7 items of 27 documents

Beta-amyloid monomers are neuroprotective

2009

The 42-aa-long β-amyloid protein—Aβ1-42—is thought to play a central role in the pathogenesis of Alzheimer's disease (AD) (Walsh and Selkoe, 2007). Data from AD brain (Shankar et al., 2008), transgenic APP (amyloid precursor protein)-overexpressing mice (Lesné et al., 2006), and neuronal cultures treated with synthetic Aβ peptides (Lambert et al., 1998) indicate that self-association of Aβ1-42monomers into soluble oligomers is required for neurotoxicity. The function of monomeric Aβ1-42is unknown. The evidence that Aβ1-42is present in the brain and CSF of normal individuals suggests that the peptide is physiologically active (Shoji, 2002). Here we show that synthetic Aβ1-42monomers support …

N-MethylaspartateStimulationPeptideNeuroprotectionNeuro-degenerative diseasePathogenesismental disordersNitrilesmedicineAmyloid precursor proteinButadienesExcitatory Amino Acid AgonistsAnimalsEnzyme InhibitorsReceptorCells CulturedPodophyllotoxinchemistry.chemical_classificationCerebral CortexNeuronsAnalysis of VarianceAmyloid beta-PeptidesbiologyCell DeathDose-Response Relationship DrugGeneral NeuroscienceNeurodegenerationβ-Amyloid proteinNeurotoxicityself-assemblyTyrphostinsmedicine.diseaseEmbryo MammalianPeptide FragmentsCell biologyRatsNeuroprotective Agentschemistrybiology.proteinBrief CommunicationsNeuroscienceβ-Amyloid protein; Neuro-degenerative diseases; self-assembly
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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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The effects of glutamate receptor antagonists on cerebellar granule cell survival and development.

2007

N-Methyl-d-aspartate (NMDA) receptor stimulation promotes neuronal survival and differentiation under both in vitro and in vivo conditions. We studied the effects of various NMDA receptor antagonists acting at different NMDA receptor binding sites and non-NMDA receptor antagonists on the development and survival of cerebellar granule cell (CGC) culture. Only three of the drugs tested induced neurotoxicity-MK-801 (non-competitive NMDA channel blocking antagonist), ifenprodil (an antagonist of the NR2B site and polyamine site of the NMDA receptor) and L-701.324 (full antagonist at glycine site), while CGP-37849 (a competitive NMDA antagonist), (+)-HA-966 (a partial agonist of the glycine site…

N-MethylaspartateTime FactorsNeuriteCell SurvivalGlutamic AcidTetrazolium SaltsAMPA receptorPharmacologyBiologyToxicologyNeuroprotectionchemistry.chemical_compoundCerebellumIfenprodilExcitatory Amino Acid AgonistsIn Situ Nick-End LabelingAnimalsDrug InteractionsRats WistarCells CulturedNeuronsAnalysis of VarianceCell DeathDose-Response Relationship DrugGeneral NeuroscienceGlutamic acidRatsThiazolesnervous systemchemistryBiochemistryAnimals NewbornCompetitive antagonistNMDA receptorNBQXExcitatory Amino Acid AntagonistsNeurotoxicology
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The NMDA receptor complex: a promising target for novel antiepileptic strategies.

2001

Antiepileptic drugs (AEDs) cover a broad spectrum of pathological conditions ranging from seizures following congenital or acquired brain disorders to behavioural and psychiatric disorders and recently neuropathic pain. The need for novel antiepileptics raises from the expanding field of indications as well as from the fact, that special seizure types are refractory to common AEDs. In addition, many of the conventional antiepileptic drugs exhibit an unfavourable side-effect profile. Since there is growing evidence, that NMDA receptor activation might play a crucial role in epilepsy, NMDA receptor antagonists have become compounds of interest in preventing and treating seizures. This review …

N-Methylaspartatemedicine.medical_treatmentPharmacologyBiochemistryReceptors N-Methyl-D-AspartateFelbamatechemistry.chemical_compoundEpilepsyDrug DiscoveryIfenprodilmedicineAnimalsHumansRemacemidePharmacologyEpilepsybusiness.industryOrganic ChemistryMemantinemedicine.diseaseDizocilpineAnticonvulsantchemistryMolecular MedicineAnticonvulsantsbusinessEliprodilmedicine.drugCurrent medicinal chemistry
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Action of anticonvulsants on hippocampal slices in Mg-free medium

1989

The effects of six prototype anticonvulsant drugs were investigated on epileptiform field potential discharges evoked in hippocampal slices of rats by removing magnesium ions from the perfusion fluid in order to reveal a possible interaction with N-methyl-D-aspartate (NMDA) receptor activation. All drugs reduced the multiple discharges with the following order of potency: midazolam greater than carbamazepine = phenytoin = phenobarbital greater than ethosuximide = valproate. They had a stronger depressant effect on the later population spikes but none of them abolished the epileptiform discharge. These effects can be explained by known mechanisms of action of the anticonvulsants tested and l…

N-Methylaspartatemedicine.medical_treatmentPopulationPyramidal TractsIn Vitro TechniquesPharmacologyHippocampusReceptors N-Methyl-D-AspartatemedicineAnimalsMagnesiumeducationMagnesium ionPharmacologyAspartic Acideducation.field_of_studyEpilepsyDose-Response Relationship DrugChemistryElectroencephalographyRats Inbred StrainsGeneral MedicineCarbamazepineElectric StimulationRatsReceptors NeurotransmitterPerfusionEthosuximideAnticonvulsantnervous systemMechanism of actionNMDA receptorAnticonvulsantsPhenobarbitalmedicine.symptommedicine.drugNaunyn-Schmiedeberg's Archives of Pharmacology
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The triaminopyridine flupirtine prevents cell death in rat cortical cells induced by N-methyl-D-aspartate and gp120 of HIV-1.

1994

Abstract Flupirtine, a triaminopyridine derivative, is a non-opiate centrally acting analgesic agent with muscle relaxant properties. Now we show that this drug displays a potent cytoprotective effect on neurons (rat cortical cells) treated with (i) the excitatory amino acid N-methyl- d -aspartate (NMDA) or (ii) with the human immunodeficiency virus type 1 (HIV-1) coat protein gp120. In the absence of the drug the two agents cause a >90% reduction of cell viability after a 18 h incubation. During this period the DNA in the cells undergoes fragmentation and shows a pattern which is typical for cell death. If the neurons were preincubated with flupirtine for 2 h and subsequently exposed to th…

Programmed cell deathAIDS Dementia ComplexN-Methylaspartatemedicine.drug_classCell SurvivalAnalgesicAminopyridinesBiologyPharmacologyHIV Envelope Protein gp120medicineAnimalsViability assayFragmentation (cell biology)Rats WistarCells CulturedPharmacologyCerebral CortexNeuronsAnalgesicsCell DeathMuscle relaxantRatsMolecular Weightmedicine.anatomical_structureImmunologyHIV-1NMDA receptorNeuronFlupirtinemedicine.drugEuropean journal of pharmacology
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Excitotoxin-induced changes in transglutaminase during differentiation of cerebellar granule cells

2002

Excitotoxicity induced by NMDA receptor stimulation is able to increase the activity of many enzymes involved in neuronal cell death. Primary cultures of rat cerebellar granule cells were used to elucidate the role of transglutaminase reaction in the excitotoxic cell response, and to evaluate the role of glutamate receptors in cell survival and degeneration. Granule neurons, maintained in vitro for two weeks, were exposed to NMDA at different stages of differentiation. Following NMDA receptor activation, increases in transglutaminase activity were observed in cell cultures. The levels of enzyme activity were higher in cells at 5 days in vitro than in those at 8-9 or 13-14 days in vitro. Mor…

Programmed cell deathN-MethylaspartateTime FactorsCell SurvivalTissue transglutaminaseNeurotoxinsClinical BiochemistryExcitotoxicityStimulationmedicine.disease_causeReceptors N-Methyl-D-AspartateBiochemistryCerebellummedicineAnimalsRats WistarNeuronsTransglutaminasesbiologyOrganic ChemistryGlutamate receptorCell DifferentiationIn vitroRatsCell biologyAnimals Newbornnervous systemApoptosisNerve Degenerationbiology.proteinNMDA receptorTransglutaminase – Excitotoxicity – Neurodegenerative diseases – Apoptosis – Glutamate – Cerebellar granule neuronsAmino Acids
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