1996
Cytoskeletal Breakdown and Apoptosis Elicited by NO Donors in Cerebellar Granule Cells Require NMDA Receptor Activation
Bonfoco E, Leist M, Zhivotovsky B, Orrenius S, Lipton S, Nicotera P. Cytoskeletal Breakdown and Apoptosis Elicited by NO Donors in Cerebellar Granule Cells Require NMDA Receptor Activation. Journal Of Neurochemistry 1996, 67: 2484-2493. PMID: 8931482, DOI: 10.1046/j.1471-4159.1996.67062484.x.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisAstrocytesCalciumCells, CulturedCerebellumCysteineCytoskeletonDizocilpine MaleateDNA FragmentationEnzyme InhibitorsExcitatory Amino Acid AntagonistsNitric OxidePenicillaminePotassiumRatsRats, Sprague-DawleyReceptors, N-Methyl-D-AspartateSignal TransductionS-Nitroso-N-AcetylpenicillamineS-NitrosothiolsTyrosineConceptsCultured cerebellar granule cellsNMDA receptor activationCerebellar granule cellsCytoskeletal breakdownGranule cellsReceptor activationUncompetitive NMDA receptor antagonistsD-aminophosphonovaleric acidNecrosis of neuronsS-nitrosocysteineNO donor S-nitrosocysteineNMDA receptor antagonistNitric oxide donorTyrosine nitrationReceptor antagonistMK-801Astroglial cellsOxide donorIntracellular Ca2NO donorBreakdown of microtubulesCerebellar astroglial cellsApoptosisUnderwent apoptosisCytoskeletal alterations
1992
Open-channel block of N-methyl-D-aspartate (NMDA) responses by memantine: therapeutic advantage against NMDA receptor-mediated neurotoxicity
Chen H, Pellegrini J, Aggarwal S, Lei S, Warach S, Jensen F, Lipton. Open-channel block of N-methyl-D-aspartate (NMDA) responses by memantine: therapeutic advantage against NMDA receptor-mediated neurotoxicity. Journal Of Neuroscience 1992, 12: 4427-4436. PMID: 1432103, PMCID: PMC6576016, DOI: 10.1523/jneurosci.12-11-04427.1992.Peer-Reviewed Original ResearchConceptsNMDA receptor-mediated neurotoxicityMK-801Open channel blockTherapeutic advantageLow micromolar concentrationsNMDA open-channel blockersHypoxic-ischemic brain injuryN-methyl-D-aspartate (NMDA) responsesTherapeutic potentialRetinal ganglion cell neuronsRat stroke modelGanglion cell neuronsLevels of glutamateNMDA receptor stimulationCultures of ratConsiderable therapeutic potentialMechanism of actionOpen channel blockerMicromolar concentrationsClinical entityBrain injuryNMDA antagonistsNMDA receptorsExcessive activationStroke model
1990
Comparison of delayed administration of competitive and uncompetitive antagonists in preventing NMDA receptor-mediated neuronal death.
Levy D, Lipton S. Comparison of delayed administration of competitive and uncompetitive antagonists in preventing NMDA receptor-mediated neuronal death. Neurology 1990, 40: 852-5. PMID: 1970428, DOI: 10.1212/wnl.40.5.852.Peer-Reviewed Original ResearchConceptsMK-801Uncompetitive antagonistCompetitive antagonistNMDA receptor-mediated neuronal deathN-methyl-D-aspartate receptorsRetinal ganglion cell neuronsStudies of excitotoxicityGanglion cell neuronsGlutamate-induced injuryNeuronal cell deathUncompetitive NMDA antagonistsHypoxia-ischemiaNeurologic injuryProtective dosesNeuronal deathCentral neuronsInitial insultNMDA antagonistsProtective effectCell neuronsAntagonistMinutes of exposureToxic damageInjuryCell death
1988
Central mammalian neurons normally resistant to glutamate toxicity are made sensitive by elevated extracellular Ca2+: toxicity is blocked by the N-methyl-D-aspartate antagonist MK-801.
Hahn J, Aizenman E, Lipton S. Central mammalian neurons normally resistant to glutamate toxicity are made sensitive by elevated extracellular Ca2+: toxicity is blocked by the N-methyl-D-aspartate antagonist MK-801. Proceedings Of The National Academy Of Sciences Of The United States Of America 1988, 85: 6556-6560. PMID: 2901101, PMCID: PMC282012, DOI: 10.1073/pnas.85.17.6556.Peer-Reviewed Original ResearchConceptsAntagonist MK-801MK-801N-methyl-D-aspartate (NMDA) receptor-coupled ion channelsExtracellular Ca2N-methyl-D-aspartate antagonist MK-801Rat retinal ganglion cellsReceptor-coupled ion channelsGlutamate-induced cell deathCentral mammalian neuronsRetinal ganglion cellsElevated extracellular Ca2Severe neurological insultPatch-clamp experimentsDementia complexNeuronal deathCentral neuronsGanglion cellsNeurological insultNeurotoxic effectsAlzheimer's diseaseNeurological disordersDegenerative disordersNerve cellsMammalian neuronsHuntington's diseaseThe interaction of agonists and noncompetitive antagonists at the excitatory amino acid receptors in rat retinal ganglion cells in vitro
Karschin A, Aizenman E, Lipton. The interaction of agonists and noncompetitive antagonists at the excitatory amino acid receptors in rat retinal ganglion cells in vitro. Journal Of Neuroscience 1988, 8: 2895-2906. PMID: 2842467, PMCID: PMC6569411, DOI: 10.1523/jneurosci.08-08-02895.1988.Peer-Reviewed Original ResearchConceptsExcitatory amino acidsGanglion cellsMK-801Excitatory amino acid receptorsRat retinal ganglion cellsWhole-cell patch-clamp techniqueCultured ganglion cellsKainate-activated currentsKainate-induced currentsAmino acid receptorsConcentrations of NMDAApplication of kainateKainate-induced responsesPresence of NMDAReceptor-ion channel complexRetinal ganglion cellsNoncompetitive NMDA antagonistPatch-clamp techniqueDegree of blockAnticonvulsant MK-801Ganglion cell membraneDissociative anesthetic phencyclidineMicroM kainateKainate currentsLarge inward currents