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
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