2014
Concept of Excitotoxicity via Glutamate Receptors
Piña-Crespo J, Sanz-Blasco S, Lipton S. Concept of Excitotoxicity via Glutamate Receptors. 2014, 1015-1038. DOI: 10.1007/978-1-4614-5836-4_125.Peer-Reviewed Original ResearchDownstream intracellular signaling cascadesIntracellular signaling cascadesGlutamate receptorsPattern of expressionUncovering genesNeuroprotective therapiesIntracellular effectorsSignaling cascadesCell injuryMolecular mechanismsSecond messengerGlutamate receptor overactivationMolecular biologyDisease statesCell deathNeuropsychiatric diseasesNitric oxideInositol phospholipidsAmino acidsCell surfaceConcept of excitotoxicityPotential neuroprotective therapiesExcitatory amino acidsGlutamate-mediated neurotoxicityNerve cell injury
2008
Clinically Tolerated Strategies for NMDA Receptor Antagonism
Vincent Chen H, Zhang D, Lipton S. Clinically Tolerated Strategies for NMDA Receptor Antagonism. The Receptors 2008, 327-361. DOI: 10.1007/978-1-59745-055-3_8.Peer-Reviewed Original ResearchExcessive NMDAR activityNMDAR activityClinical trialsGlutamate receptorsSide effectsNeurologic disordersNervous systemAcute hypoxic-ischemic brain injuryGeneralized inhibitionAlzheimer's diseaseSecond-generation memantine derivativesHypoxic-ischemic brain injuryPhase 3 clinical trialsExcessive NMDAR activationSevere neuropathic painExcitatory amino acidsGlutamate-mediated neurotoxicityGlutamate receptor subtypesChronic neurodegenerative diseasesSystemic side effectsMajor excitatory transmitterNormal functionNMDA receptor antagonismGreater neuroprotective propertiesCentral nervous system
1999
Neuroprotection by the NMDA receptor-associated open-channel blocker memantine in a photothrombotic model of cerebral focal ischemia in neonatal rat
Stieg P, Sathi S, Warach S, Le D, Lipton S. Neuroprotection by the NMDA receptor-associated open-channel blocker memantine in a photothrombotic model of cerebral focal ischemia in neonatal rat. European Journal Of Pharmacology 1999, 375: 115-120. PMID: 10443569, DOI: 10.1016/s0014-2999(99)00214-9.Peer-Reviewed Original ResearchConceptsMagnetic resonance imagingSide effectsInfarct sizeNeonatal ratsChannel blockersNMDA receptorsFocal cerebral ischemia modelNeurobehavioral side effectsIschemic brain injuryEffects of memantineExcitatory amino acidsInduction of strokeRodent stroke modelsAdult animal modelsCerebral ischemia modelSubstantial side effectsCerebral focal ischemiaNumerous side effectsNeuronal cell culturesNeonatal neuronsPhotochemical thrombosisPhotothrombotic modelNeuronal injuryCerebral ischemiaFocal ischemia
1997
Molecular basis of glutamate toxicity in retinal ganglion cells
Sucher N, Lipton S, Dreyer E. Molecular basis of glutamate toxicity in retinal ganglion cells. Vision Research 1997, 37: 3483-3493. PMID: 9425525, DOI: 10.1016/s0042-6989(97)00047-3.Peer-Reviewed Original ResearchConceptsRetinal ganglion cellsExcitatory amino acidsNMDA receptor antagonistRetinal ischemiaReceptor antagonistGanglion cellsGlutamate toxicityAnterior ischemic optic neuropathyN-methyl-D-aspartate (NMDA) subtypeNMDA receptor-mediated toxicityNon-NMDA receptor subtypesAcute vascular insultCentral artery occlusionOptic nerve traumaIschemic optic neuropathyGlutamate-induced neurotoxicitySelective NMDA receptor antagonistGlutamate-induced depolarizationVoltage-gated Ca2Amino acid glutamateOptic neuritisNerve traumaArtery occlusionFuture clinical useNeuronal lossAbsence of excitotoxicity-induced apoptosis in the hippocampus of mice lacking the Jnk3 gene
Yang D, Kuan C, Whitmarsh A, Rinócn M, Zheng T, Davis R, Rakic P, Flavell R. Absence of excitotoxicity-induced apoptosis in the hippocampus of mice lacking the Jnk3 gene. Nature 1997, 389: 865-870. PMID: 9349820, DOI: 10.1038/39899.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisDrug ResistanceExcitatory Amino Acid AgonistsGene ExpressionGene TargetingGlutamic AcidHippocampusKainic AcidMiceMice, Inbred C57BLMice, KnockoutMitogen-Activated Protein Kinase 10Mitogen-Activated Protein KinasesNeuronsPhosphorylationProtein KinasesProtein Serine-Threonine KinasesProtein-Tyrosine KinasesProto-Oncogene Proteins c-fosProto-Oncogene Proteins c-junSeizuresSignal TransductionTranscription Factor AP-1ConceptsKainic acidGlutamate receptor agonist kainic acidAgonist kainic acidExcitotoxicity-induced apoptosisExcitatory amino acidsHippocampal neuron apoptosisHippocampus of miceStress-induced neuronal apoptosisObserved neuroprotectionGlutamate neurotoxicitySeizure activityNeuron apoptosisGlutamate toxicityNeuronal apoptosisAP-1 transcription factor complexJNK3 geneMutant miceMiceMembrane depolarizationNoxious stressTranscription factor complexApoptosisC-JunRecent studiesTranscriptional activityEvidence Showing That β-Endorphin Regulates Cyclic Guanosine 3′,5′-Monophosphate (cGMP) Efflux: Anatomical and Functional Support for an Interaction between Opiates and Nitric Oxide*
Pu S, Horvath T, Diano S, Naftolin F, Kalra P, Kalra S. Evidence Showing That β-Endorphin Regulates Cyclic Guanosine 3′,5′-Monophosphate (cGMP) Efflux: Anatomical and Functional Support for an Interaction between Opiates and Nitric Oxide*. Endocrinology 1997, 138: 1537-1543. DOI: 10.1210/en.138.4.1537.Peer-Reviewed Original ResearchN-methyl-D-aspartateExcitatory amino acidsCyclic guanosine 3',5'-monophosphateMedial preoptic areaOpioid influenceGnRH secretionNitric oxideExcitatory N-methyl-D-aspartateN-methyl-D-aspartate receptorsPreoptic areaInhibitory opioid influenceB-endorphinOpiate receptor antagonistNOS-immunoreactive neuronsPituitary LH secretionNO releaseStimulation of NO releaseRelease of GnRHSubpopulations of neuronsGuanosine 3',5'-monophosphateCentral nervous systemReceptor agonistsReceptor antagonistEndogenous opioidsHypothalamic sectionsEvidence Showing That β-Endorphin Regulates Cyclic Guanosine 3′,5′-Monophosphate (cGMP) Efflux: Anatomical and Functional Support for an Interaction between Opiates and Nitric Oxide
Pu S, Horvath TL, Diano S, Naftolin F, Kalra PS, Kalra SP. Evidence Showing That β-Endorphin Regulates Cyclic Guanosine 3′,5′-Monophosphate (cGMP) Efflux: Anatomical and Functional Support for an Interaction between Opiates and Nitric Oxide. Endocrinology 1997, 138: 1537-1543. PMID: 9075713, DOI: 10.1210/endo.138.4.5086.Peer-Reviewed Original ResearchConceptsExcitatory amino acidsMedial preoptic areaCGMP/Opioid influenceGnRH secretionNitric oxidePreoptic areaN-methyl-D-aspartate receptorsMu-opiate receptor agonistNOS-immunopositive cellsNOS-immunoreactive neuronsPituitary LH secretionOpiate receptor agonistsOpiate receptor antagonistRelease of GnRHCentral nervous systemDirect inhibitory controlExcitatory NMDATonic restraintLH secretionEndogenous opioidsNOS pathwayReceptor antagonistBeta-endorphinGonadal steroids
1996
AIDS Dementia as a Form of Excitotoxicity: Potential Therapy with NMDA Open-Channel Blockers and Redox Congeners of Nitric Oxide
Lipton S. AIDS Dementia as a Form of Excitotoxicity: Potential Therapy with NMDA Open-Channel Blockers and Redox Congeners of Nitric Oxide. Gwumc Department Of Biochemistry And Molecular Biology Annual Spring Symposia 1996, 341-356. DOI: 10.1007/978-1-4899-0209-2_41.Peer-Reviewed Original ResearchRedox modulatory siteNMDA receptorsOpen channel blockerNeuronal injuryNeuronal damageN-methyl-D-aspartate (NMDA) receptor-operated channelsModulatory siteNMDA open-channel blockersNitric oxideHIV-1 envelope protein gp120Forms of excitotoxicityAIDS dementia complexHIV-1 resultsExcitatory amino acidsMacrophages/microgliaExistence of HIVReceptor-operated channelsFuture pharmacological interventionsFinal common pathwayAmyotrophic lateral sclerosisEnvelope protein gp120Platelet-activating factorReceptor/channel complexNormal neuronal functionNMDA receptor/channel complex
1995
The Coat Protein gp120 of HIV‐1 Inhibits Astrocyte Uptake of Excitatory Amino Acids via Macrophage Arachidonic Acid
Dreyer E, Lipton S. The Coat Protein gp120 of HIV‐1 Inhibits Astrocyte Uptake of Excitatory Amino Acids via Macrophage Arachidonic Acid. European Journal Of Neuroscience 1995, 7: 2502-2507. PMID: 8845955, DOI: 10.1111/j.1460-9568.1995.tb01048.x.Peer-Reviewed Original ResearchConceptsExcitatory amino acidsAmino acidsAstrocyte uptakeNeuronal damageProtein gp120Excitatory amino acid uptakeAmino acid uptakeN-methyl-D-aspartate receptorsArachidonic acidCentral mammalian neuronsMammalian neuronsReleases arachidonic acidNeuronal injuryBrain macrophagesImmunodeficiency syndromeNeurological dysfunctionAcid uptakeExcess glutamateGp120MacrophagesAstrocytesNeuronsInitial activationPresent dataUptakeNitric oxide synthase inhibition and extracellular glutamate concentration after cerebral ischemia/reperfusion.
Zhang J, Benveniste H, Klitzman B, Piantadosi C. Nitric oxide synthase inhibition and extracellular glutamate concentration after cerebral ischemia/reperfusion. Stroke 1995, 26: 298-304. PMID: 7530389, DOI: 10.1161/01.str.26.2.298.Peer-Reviewed Original ResearchConceptsIschemia/reperfusionBlood-brain barrierCerebral blood flowBrain ischemia/reperfusionExcitatory amino acidsExtracellular glutamate concentrationL-NAMEBlood flowGlutamate concentrationSynthase inhibitionL-arginineExcitatory amino acid toxicityL-NAME-treated ratsPostischemic cerebral blood flowNitric oxide synthase inhibitionCerebral ischemia/reperfusionBlood-brain barrier functionL-arginine methyl esterCerebral blood flow responseBlood-brain barrier permeabilityGlobal brain ischemia/reperfusionElevated glutamate concentrationsImmediate postischemic periodInterstitial glutamate concentrationL-NAME administration
1993
Depolarization inactivation of dopamine neurons: Terminal release characteristics
Moghaddam B, Bunney B. Depolarization inactivation of dopamine neurons: Terminal release characteristics. Synapse 1993, 14: 195-200. PMID: 8105547, DOI: 10.1002/syn.890140302.Peer-Reviewed Original ResearchConceptsExtracellular dopamine levelsChronic haloperidol treatmentDopamine levelsHaloperidol treatmentExtracellular levelsPerfusion of tetrodotoxinExcitatory amino acidsStriatal extracellular levelsVehicle-treated animalsExtracellular glutamate levelsHaloperidol-treated animalsMedial forebrain bundleStriatal dopamine systemGroups of animalsExogenous antagonistsChronic haloperidolChronic treatmentDepolarization inactivationExcitatory actionBasal outflowDopamine neuronsGlutamate levelsImpulse flowForebrain bundleMicrodialysis techniqueDelayed administration of memantine prevents N‐methyl‐D‐aspartate receptor‐mediated neurotoxicity
Pellegrini J, Lipton S. Delayed administration of memantine prevents N‐methyl‐D‐aspartate receptor‐mediated neurotoxicity. Annals Of Neurology 1993, 33: 403-407. PMID: 8098195, DOI: 10.1002/ana.410330414.Peer-Reviewed Original ResearchConceptsExcitatory amino acidsN-methyl-D-aspartate receptor-mediated neurotoxicityPotent N-methyl-D-aspartate antagonistNeonatal rat retinal ganglion cellsN-methyl-D-aspartate (NMDA) subtypeN-methyl-D-aspartate antagonistsRat retinal ganglion cellsImmunodeficiency syndrome (AIDS) dementiaAcute neurological conditionsHypoxia/ischemiaChronic neurodegenerative diseasesRetinal ganglion cellsNeuronal cell deathMicroM memantineAntiparkinsonian drugsCentral neuronsGanglion cellsExcessive activationGlutamate receptorsNeurological conditionsNeurodegenerative diseasesHuntington's diseaseNeurotoxicityPrimary culturesDisease
1992
Ethanol attenuates the response of locus coeruleus neurons to excitatory amino acid agonists in vivo
Engberg G, Hajós M. Ethanol attenuates the response of locus coeruleus neurons to excitatory amino acid agonists in vivo. Naunyn-Schmiedeberg's Archives Of Pharmacology 1992, 345: 222-226. PMID: 1314963, DOI: 10.1007/bf00165740.Peer-Reviewed Original ResearchConceptsLocus coeruleus neuronsCoeruleus neuronsLocus coeruleus noradrenergic neuronsExcitatory amino acid agonistsLocus coeruleus responseAmino acid agonistsExcitatory amino acidsAdministration of ethanolExtracellular recording techniquesEffects of ethanolMicroiontophoretic applicationNoradrenergic neuronsGlutamate excitationHippocampal slicesLocus coeruleusEthanol intoxicationElectrophysiological studiesEthanol treatmentFiring patternsNeuronsRecording techniquesUnderlaying mechanismPresent studyVivoKainate
1991
Excitatory amino acids and morphine withdrawal: differential effects of central and peripheral kynurenic acid administration
Rasmussen K, Krystal J, Aghajanian G. Excitatory amino acids and morphine withdrawal: differential effects of central and peripheral kynurenic acid administration. Psychopharmacology 1991, 105: 508-512. PMID: 1771218, DOI: 10.1007/bf02244371.Peer-Reviewed Original ResearchConceptsAcid administrationKynurenic acidSubcutaneous administrationPeripheral excitatory amino acid receptorsExcitatory amino acid antagonist kynurenic acidExcitatory amino acid receptorsAntagonist kynurenic acidExcitatory amino acidsAmino acid receptorsLocus coeruleus neuronsMorphine-dependent ratsBlood-brain barrierSingle-unit recordingsMorphine withdrawalCoeruleus neuronsAntagonist treatmentAbstinence symptomsOpiate withdrawalUnit recordingsAnesthetized animalsAcid receptorsBehavioral signsAdministrationDifferential effectsWithdrawalModulation of Protein Kinase C Translocation by Excitatory and Inhibitory Amino Acids in Primary Cultures of Neurons
Vaccarino F, Liljequist S, Tallman J. Modulation of Protein Kinase C Translocation by Excitatory and Inhibitory Amino Acids in Primary Cultures of Neurons. Journal Of Neurochemistry 1991, 57: 391-396. PMID: 1649249, DOI: 10.1111/j.1471-4159.1991.tb03765.x.Peer-Reviewed Original ResearchMeSH KeywordsAmino AcidsAnimalsAnimals, NewbornBicucullineCell MembraneCells, CulturedCerebral CortexCorpus StriatumDizocilpine MaleateGlutamatesKineticsNeuronsOxadiazolesPhorbol 12,13-DibutyrateProtein Kinase CRatsRats, Inbred StrainsReceptors, AMPAReceptors, NeurotransmitterReceptors, N-Methyl-D-AspartateTetrodotoxinConceptsProtein kinase CPKC translocationAmino acidsExtracellular mediumProtein kinase C translocationAmino acid stimulationPrimary culturesKinase CC translocationExcitatory amino acid receptorsTranslocationExcitatory amino acid stimulationImine hydrogen maleateExcitatory amino acidsAmino acid receptorsRat cerebral cortexInhibitory amino acidsNMDA receptor antagonistAbsence of calciumAcid receptorsPhysiological concentrationsCerebral cortexMetabotropic receptorsReceptor antagonistAMPA receptorsGDPβS antagonizes whole-cell current responses to excitatory amino acids
Budson A, Jackson P, Lipton S. GDPβS antagonizes whole-cell current responses to excitatory amino acids. Brain Research 1991, 548: 346-348. PMID: 1868345, DOI: 10.1016/0006-8993(91)91147-s.Peer-Reviewed Original ResearchThe excitotoxin hypothesis in relation to cerebral ischemia.
Benveniste H. The excitotoxin hypothesis in relation to cerebral ischemia. Cerebrovascular And Brain Metabolism Reviews 1991, 3: 213-45. PMID: 1931486.Peer-Reviewed Original ResearchConceptsExcitatory amino acidsSelective neuronal deathExcitotoxin hypothesisNeuronal deathExtracellular glutamate concentration increasesSelective vulnerable brain regionsBrain regionsN-methyl-D-aspartate receptorsGlutamate accumulationBrain cell injuryVulnerable brain regionsTransient global ischemiaHigh-performance liquid chromatographyDistinct brain regionsNeuronal injuryBrain extracellular spaceCerebral ischemiaTransient ischemiaAntagonist APVExcitatory neurotransmitterGlobal ischemiaExtracellular glutamateNMDA antagonistsCertain neuronsMicrodialysis technique
1990
Kynurenic acid blocks chemogenic nociception
Hajós M, Engberg G. Kynurenic acid blocks chemogenic nociception. Journal Of Pharmacy And Pharmacology 1990, 42: 373-374. PMID: 1976793, DOI: 10.1111/j.2042-7158.1990.tb05434.x.Peer-Reviewed Original Research
1988
Presynaptic actions of carbachol and adenosine on corticostriatal synaptic transmission studied in vitro
Malenka R, Kocsis J. Presynaptic actions of carbachol and adenosine on corticostriatal synaptic transmission studied in vitro. Journal Of Neuroscience 1988, 8: 3750-3756. PMID: 2848109, PMCID: PMC6569613, DOI: 10.1523/jneurosci.08-10-03750.1988.Peer-Reviewed Original ResearchConceptsStriatal neuronsSynaptic transmissionCorticostriatal synaptic transmissionExcitatory amino acidsField potentialsNeostriatal slice preparationField potential responsesCorticostriatal afferentsCorticostriatal responsesCorticostriatal fibersPresynaptic actionPostsynaptic actionsStriatal neurotransmittersCalcium antagonistsCarbachol actionCortical afferentsAfferent fibersIntrinsic neuronsStriatal afferentsPutative neurotransmittersAdenosine actionSlice preparationCorpus callosumNeostriatal slicesAfferentsThe 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
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