2025
Mutant prion protein enhances NMDA receptor activity, activates PKC, and triggers rapid excitotoxicity in mice
Lin J, Callender J, Mayfield J, McClatchy D, Ojeda-Juárez D, Pourhamzeh M, Soldau K, Kurt T, Danque G, Khuu H, Ronson J, Pizzo D, Du Y, Gruber M, Sevillano A, Wang J, Orrú C, Chen J, Funk G, Aguilar-Calvo P, Aulston B, Roy S, Rho J, Bui J, Newton A, Lipton S, Caughey B, Patrick G, Doré K, Yates J, Sigurdson C. Mutant prion protein enhances NMDA receptor activity, activates PKC, and triggers rapid excitotoxicity in mice. Journal Of Clinical Investigation 2025, 135: e186432. PMID: 40185484, PMCID: PMC12077891, DOI: 10.1172/jci186432.Peer-Reviewed Original ResearchConceptsN-methyl-D-aspartate receptorsProtein kinase CAmino terminusPrion proteinN-methyl-D-aspartateMutant prion proteinNMDA receptor activationN-linked glycosylation sitesExcitatory-inhibitory imbalanceHippocampal pyramidal neuronsDownstream signaling eventsActivate protein kinase CNMDAR channelsNeuronal hyperexcitabilityFunctional motifsGlutamate receptorsCalcium influxPhosphoproteomic analysisPyramidal neuronsGlycosylation sitesSignaling eventsReceptor activationPrion-infected miceDendritic beadingSynapse lossContrasting patterns of extrasynaptic NMDAR-GluN2B expression in macaque subgenual cingulate and dorsolateral prefrontal cortices
Joyce M, Datta D, Arellano J, Duque A, Morozov Y, Morrison J, Arnsten A. Contrasting patterns of extrasynaptic NMDAR-GluN2B expression in macaque subgenual cingulate and dorsolateral prefrontal cortices. Frontiers In Neuroanatomy 2025, 19: 1553056. PMID: 40255911, PMCID: PMC12006084, DOI: 10.3389/fnana.2025.1553056.Peer-Reviewed Original ResearchSubgenual cingulate cortexDorsolateral prefrontal cortexPrefrontal cortexPutative pyramidal neuronsN-methyl-D-aspartate receptorsN-methyl-D-aspartateSporadic Alzheimer's diseaseSubgenual cingulateCingulate cortexWorking memoryMacaque dlPFCDLPFCNMDAR antagonistsGluN2B subunitVulnerable to alterationsCortexSynaptic expressionPyramidal neuronsSynaptic functionAlzheimer's diseaseNeurodegenerative processesExtrasynaptic sitesTau pathologySchizophreniaCingulateN-methyl-d-aspartate receptor hypofunction causes recurrent and transient failures of perceptual inference
Weilnhammer V, Rothkirch M, Yilmaz D, Fritsch M, Ptasczynski L, Reichenbach K, Roediger L, Corlett P, Sterzer P. N-methyl-d-aspartate receptor hypofunction causes recurrent and transient failures of perceptual inference. Brain 2025, 148: 1531-1539. PMID: 39821016, PMCID: PMC12073972, DOI: 10.1093/brain/awaf011.Peer-Reviewed Original ResearchN-methyl-D-aspartate receptorsN-methyl-D-aspartateN-methyl-D-aspartate receptor hypofunctionS-ketamineSymptoms of schizophreniaDissociation of perceptionsHealthy human participantsExternal sensory signalsReceptor hypofunctionSensory signalsNMDAR hypofunctionPerceptual inferenceCase-control studyInternal predictionsHuman participantsPlacebo-ControlledDouble-blindCross-over experimentHypofunctionSchizophreniaParanoidPerceptionSCZ
2024
Relationship between diet and postoperative pain: A scoping review
Chowdhary H, Chow R, Li J, Rajput K. Relationship between diet and postoperative pain: A scoping review. Journal Of Anesthesia And Translational Medicine 2024, 3: 181-187. DOI: 10.1016/j.jatmed.2024.11.004.Peer-Reviewed Original ResearchPost-surgical painN-methyl-D-aspartateAcute postoperative painPostoperative painHigh-fat dietPain sensitivitySurgical populationImpact of dietIntermittent fastingPersistent post-surgical painAcute post-surgical painHuman studiesDiverse surgical populationResponse to morphinePost-operative painChronic pain conditionsHigh-fatReduction of inflammationPersistent painPain conditionsPainCochrane DatabaseRisk factorsCollate available evidenceInflammationMismatch Negativity as an Index of Auditory Short-Term Plasticity: Associations with Cortisol, Inflammation, and Gray Matter Volume in Youth at Clinical High Risk for Psychosis
Hamilton H, Roach B, Bachman P, Belger A, Carrión R, Duncan E, Johannesen J, Light G, Niznikiewicz M, Addington J, Bearden C, Cadenhead K, Cornblatt B, Perkins D, Tsuang M, Walker E, Woods S, Cannon T, Mathalon D. Mismatch Negativity as an Index of Auditory Short-Term Plasticity: Associations with Cortisol, Inflammation, and Gray Matter Volume in Youth at Clinical High Risk for Psychosis. Clinical EEG And Neuroscience 2024, 56: 46-59. PMID: 39552576, DOI: 10.1177/15500594241294035.Peer-Reviewed Original ResearchNMDAR-dependent plasticityClinical high riskGray matter volumeMismatch negativityMagnetic resonance imagingGray matter lossShort-term plasticityMMN amplitudeMatter volumeN-methyl-D-aspartateHigh riskCHR-PPro-inflammatory cytokine levelsPathogenesis of schizophreniaModel of schizophreniaBiomarkers of schizophreniaMismatch negativity amplitudeCHR-P individualsNorth American Prodrome Longitudinal StudyEvent-related potentialsAberrant neurodevelopmental processesInfluence of psychosisSubcortical gray matter volumesTotal gray matter volumeNMDAR hypofunctionN-Methyl-d-Aspartate Receptor Antibody and Sensory Gating Deficits in Non-smoking, Minimal Antipsychotic Medication Exposure, and First-Episode Patients With Schizophrenia
Tong J, Yang K, Li W, Wang L, Yin Y, Zhou Y, Huang J, Zhang P, Zhao Y, Chen S, Fan H, Cui Y, Luo X, Tan S, Wang Z, Feng W, Tian B, Li C, Hong L, Tan Y. N-Methyl-d-Aspartate Receptor Antibody and Sensory Gating Deficits in Non-smoking, Minimal Antipsychotic Medication Exposure, and First-Episode Patients With Schizophrenia. Schizophrenia Bulletin 2024, sbae180. PMID: 39406395, DOI: 10.1093/schbul/sbae180.Peer-Reviewed Original ResearchFirst-episode schizophreniaSensory gating deficitsN-methyl-D-aspartate receptorsFirst-episode schizophrenia groupGating deficitsN-methyl-D-aspartateP50 ratioSensory gatingExposure to antipsychotic medicationAb levelsHealthy controlsAntipsychotic medication exposureFirst-episode patientsDiagnosis of schizophreniaImpaired sensory gatingP50 sensory gating deficitN-methyl-D-aspartate receptor antibodiesAntipsychotic medicationFirst-episodeNon-smoking healthy controlsP50 differenceSchizophreniaPartial correlation analysisEnzyme-linked immunosorbent assayDeficitsGenomic insights into the comorbidity between type 2 diabetes and schizophrenia
Arruda A, Khandaker G, Morris A, Smith G, Huckins L, Zeggini E. Genomic insights into the comorbidity between type 2 diabetes and schizophrenia. Schizophrenia 2024, 10: 22. PMID: 38383672, PMCID: PMC10881980, DOI: 10.1038/s41537-024-00445-5.Peer-Reviewed Original ResearchBody mass indexType 2 diabetesType 2 diabetes riskEffect of body mass indexPutative effector genesN-methyl-D-aspartatePublic health challengeIncreased Body Mass IndexLipid-related pathwaysRisk-increasing effectMulti-omics dataMendelian randomizationPotential causal relationshipGene expression studiesDirection of effectMental healthDrug repurposing opportunitiesAssociation signalsGenomic lociGenomic insightsHealth challengesEffector genesGenetic liabilityMass indexExpression studies
2021
HMGB1, neuronal excitability and epilepsy
Dai S, Zheng Y, Wang Y, Chen Z. HMGB1, neuronal excitability and epilepsy. Acta Epileptologica 2021, 3: 13. DOI: 10.1186/s42494-021-00048-y.Peer-Reviewed Original ResearchN-methyl-D-aspartateModulation of neuronal excitabilityAnimal models of epilepsyToll-like receptor 4Antiepileptic drug therapyInterleukin (IL)-1bTranslocation of HMGB1Multiple animal modelsDevelopment of epilepsyAnti-epileptic drugsMobility group protein B1HMGB1-related pathwayModels of epilepsyNuclear factor kappa BPotential of HMGB1Advanced glycation end productsFactor kappa BGlycation end productsNeuronal excitabilityBlocking HMGB1Downstream Signaling PathwaysGlutamate receptorsHMGB1 signalingHyperexcitable neuronsDrug therapy
2020
Memantine Protects From Exacerbation of Ischemic Stroke and Blood Brain Barrier Disruption in Mild But Not Severe Hyperhomocysteinemia
Gu S, Sonkar V, Katare P, Kumar R, Kruger W, Arning E, Bottiglieri T, Lentz S, Dayal S. Memantine Protects From Exacerbation of Ischemic Stroke and Blood Brain Barrier Disruption in Mild But Not Severe Hyperhomocysteinemia. Journal Of The American Heart Association 2020, 9: e013368. PMID: 32067580, PMCID: PMC7070222, DOI: 10.1161/jaha.119.013368.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBlood-Brain BarrierCell DeathCells, CulturedCystathionine beta-SynthaseDisease Models, AnimalDisease ProgressionExcitatory Amino Acid AntagonistsHomocysteineHomocystinuriaHyperhomocysteinemiaInfarction, Middle Cerebral ArteryMemantineMice, KnockoutNeuronsNeuroprotective AgentsReceptors, N-Methyl-D-AspartateSeverity of Illness IndexConceptsN-methyl-D-aspartatePlasma total homocysteineBlood-brain barrier disruptionTotal homocysteineBrain barrier disruptionIschemic strokeN-methyl-D-aspartate receptor antagonismBarrier disruptionCerebrovascular injuryN-methyl-D-aspartate receptor antagonistExpression of NR2B subunitN-methyl-D-aspartate receptor subunitsExpression of N-methyl-D-aspartate receptor subunitsN-methyl-D-aspartate receptor antagonist memantineCystathionine beta-synthaseEffects of memantineCerebral infarct sizeTargeted treatment strategiesAcute ischemic strokeBlood-brain barrierReceptor antagonismNR2B subunitReceptor antagonistSevere elevationHomocysteine levels
2017
Seroprevalence survey of selective anti-neuronal autoantibodies in patients with first-episode schizophrenia and chronic schizophrenia
Chen C, Cheng M, Liu C, Liu C, Lin K, Hwu H. Seroprevalence survey of selective anti-neuronal autoantibodies in patients with first-episode schizophrenia and chronic schizophrenia. Schizophrenia Research 2017, 190: 28-31. PMID: 28341002, DOI: 10.1016/j.schres.2017.03.012.Peer-Reviewed Original ResearchConceptsAnti-neuronal autoantibodiesLeucine-rich glioma-inactivated-1N-methyl-D-aspartateContactin-associated protein-like 2First-episode schizophreniaAnti-NMDA receptor autoantibodiesA-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acidAssociated with psychiatric disordersGlioma-inactivated-1Blood samplesNeuronal cell surface proteinsArchived blood samplesNeuronal surface proteinsCerebral spinal fluidProtein-like 2Chronic schizophreniaReceptor autoantibodiesClinical presentationAutoimmune encephalopathyTreatment resistancePsychiatric disordersCorrect diagnosisSchizophreniaAutoantibodiesSpinal fluid
2010
Prevention of ketamine-induced working memory impairments by AMPA potentiators in a nonhuman primate model of cognitive dysfunction
Roberts B, Holden D, Shaffer C, Seymour P, Menniti F, Schmidt C, Williams G, Castner S. Prevention of ketamine-induced working memory impairments by AMPA potentiators in a nonhuman primate model of cognitive dysfunction. Behavioural Brain Research 2010, 212: 41-48. PMID: 20347881, DOI: 10.1016/j.bbr.2010.03.039.Peer-Reviewed Original ResearchMeSH Keywordsalpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic AcidAnalysis of VarianceAnimalsAnimals, NewbornArea Under CurveDisease Models, AnimalDose-Response Relationship, DrugDrug Administration ScheduleExcitatory Amino Acid AgonistsKetamineMacaca fascicularisMacaca mulattaMemory DisordersMemory, Short-TermMotor ActivityNeuropsychological TestsReaction TimeSulfonamidesThiophenesTime FactorsConceptsCognitive impairment associated with schizophreniaAlpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acidMemory impairmentN-methyl-D-aspartateCognitive dysfunctionCore aspect of schizophreniaEffects of acute ketamineBehavioral effects of ketaminePositive modulators of AMPA receptorsEffects of positive allosteric modulatorsModel of cognitive dysfunctionAlpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid receptorsNegative-like symptomsWorking Memory DeficitsWorking memory impairmentModulation of AMPA receptorsEffects of ketaminePositive allosteric modulatorsRegulation of NMDA receptorsGlutamatergic synaptic transmissionAcute ketamineWorking memoryPF-4778574Antagonist ketamineMemory deficits
1997
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*
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 sections
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