2025
S-Nitrosylation of CRTC1 in Alzheimer’s disease impairs CREB-dependent gene expression induced by neuronal activity
Zhang X, Vlkolinsky R, Wu C, Dolatabadi N, Scott H, Prikhodko O, Zhang A, Blanco M, Lang N, Piña-Crespo J, Nakamura T, Roberto M, Lipton S. S-Nitrosylation of CRTC1 in Alzheimer’s disease impairs CREB-dependent gene expression induced by neuronal activity. Proceedings Of The National Academy Of Sciences Of The United States Of America 2025, 122: e2418179122. PMID: 40014571, PMCID: PMC11892585, DOI: 10.1073/pnas.2418179122.Peer-Reviewed Original ResearchConceptsActivity-dependent gene expressionGene expressionAlzheimer's diseaseCREB-dependent gene expressionS-nitrosylationNitric oxide (NO)-related speciesTargets of S-nitrosylationNeuronal activity-dependent gene expressionPathogenesis of ADDecreased neurite lengthIncreased neuronal cell deathNeuronal cell deathSynaptic plasticityTranscriptional pathwaysCell deathCRISPR/Cas9 techniqueTranscription coactivator 1AD modelLong-term memory formationIncreased S-nitrosylationLong-term potentiationTherapeutic targetExpressionNeurite lengthCerebrocortical neurons
2023
Restorative effect of NitroSynapsin on synaptic plasticity in an animal model of depression
Tse W, Pochwat B, Szewczyk B, Misztak P, Bobula B, Tokarski K, Worch R, Czarnota-Bojarska M, Lipton S, Zaręba-Kozioł M, Bijata M, Wlodarczyk J. Restorative effect of NitroSynapsin on synaptic plasticity in an animal model of depression. Neuropharmacology 2023, 241: 109729. PMID: 37797736, DOI: 10.1016/j.neuropharm.2023.109729.Peer-Reviewed Original ResearchConceptsMedial prefrontal cortexLong-term potentiationChronic restraint stress mouse modelSynaptic plasticityN-methyl-D-aspartate receptor antagonistRestraint stress mouse modelMale C57BL/6J miceAntidepressant-like activityTail suspension testStress mouse modelFunctional synaptic plasticityMajor depressive disorderAntidepressant potentialPharmacological treatmentPsychotomimetic effectsReceptor antagonistC57BL/6J miceDepressive behaviorSucrose preferenceDepressive disorderNitroSynapsinMouse modelSuspension testBehavioral disturbancesCerebrocortical neurons
1998
Neuroprotective concentrations of the N-methyl-D-aspartate open-channel blocker memantine are effective without cytoplasmic vacuolation following post-ischemic administration and do not block maze learning or long-term potentiation
Chen H, Wang Y, Rayudu P, Edgecomb P, Neill J, Segal M, Lipton S, Jensen F. Neuroprotective concentrations of the N-methyl-D-aspartate open-channel blocker memantine are effective without cytoplasmic vacuolation following post-ischemic administration and do not block maze learning or long-term potentiation. Neuroscience 1998, 86: 1121-1132. PMID: 9697119, DOI: 10.1016/s0306-4522(98)00163-8.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBody TemperatureBrain IschemiaCytoplasmExcitatory Amino Acid AntagonistsExcitatory Postsynaptic PotentialsIn Vitro TechniquesLong-Term PotentiationMaleMaze LearningMemantineMicroscopy, ElectronNeuronsNeuroprotective AgentsRatsRats, Sprague-DawleyReceptors, N-Methyl-D-AspartateVacuolesConceptsN-methyl-D-aspartate antagonistsLong-term potentiationAspartate antagonistDizocilpine maleateSide effectsUncompetitive N-methyl-D-aspartate antagonistsN-methyl-D-aspartate blockersMorris water maze performancePost-ischemic administrationHypoxia/ischemiaExcitatory postsynaptic currentsN-methyl-D-aspartate (NMDA) channelsAdverse side effectsWater maze performanceHuman CNS disordersExcitotoxic disordersNeuroprotective concentrationsClinical tolerabilityNeuroprotective dosesClinical efficacyInfarct sizePostsynaptic currentsHippocampal slicesCNS disordersAdult rats
This site is protected by hCaptcha and its Privacy Policy and Terms of Service apply