2022
Pharmacological Mechanism of the Non-hallucinogenic 5‑HT2A Agonist Ariadne and Analogs
Cunningham M, Bock H, Serrano I, Bechand B, Vidyadhara D, Bonniwell E, Lankri D, Duggan P, Nazarova A, Cao A, Calkins M, Khirsariya P, Hwu C, Katritch V, Chandra S, McCorvy J, Sames D. Pharmacological Mechanism of the Non-hallucinogenic 5‑HT2A Agonist Ariadne and Analogs. ACS Chemical Neuroscience 2022, 14: 119-135. PMID: 36521179, PMCID: PMC10147382, DOI: 10.1021/acschemneuro.2c00597.Peer-Reviewed Original ResearchConceptsHead-twitch responseParkinson's diseaseHallucinogenic effectsTherapeutic effectTherapeutic potentialClinical therapeutic effectSevere motor deficitsNew drug classesRemarkable therapeutic effectsConsiderable therapeutic potentialComplete remissionRapid remissionMotor deficitsNeurological indicationsTwitch responseClinical resultsReceptor agonistClinical trialsPharmacological mechanismsDrug classesDopamine receptorsMembrane monoamine transporterPreclinical resultsPlasma membrane monoamine transporterGeriatric subjects
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
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