2012
Repeated Stress Causes Cognitive Impairment by Suppressing Glutamate Receptor Expression and Function in Prefrontal Cortex
Yuen EY, Wei J, Liu W, Zhong P, Li X, Yan Z. Repeated Stress Causes Cognitive Impairment by Suppressing Glutamate Receptor Expression and Function in Prefrontal Cortex. Neuron 2012, 73: 962-977. PMID: 22405206, PMCID: PMC3302010, DOI: 10.1016/j.neuron.2011.12.033.Peer-Reviewed Original ResearchMeSH Keywords2-Amino-5-phosphonovalerate6-Cyano-7-nitroquinoxaline-2,3-dioneAnalysis of VarianceAnimalsBicucullineCognition DisordersDisease Models, AnimalEndosomal Sorting Complexes Required for TransportExcitatory Amino Acid AntagonistsExcitatory Postsynaptic PotentialsF-Box ProteinsGABA-A Receptor AntagonistsImmunoprecipitationIn Vitro TechniquesMaleNedd4 Ubiquitin Protein LigasesNeuropsychological TestsPrefrontal CortexPyramidal CellsRatsRats, Sprague-DawleyReceptors, GlutamateRecognition, PsychologyRestraint, PhysicalRNA, Small InterferingStress, PsychologicalUbiquitin-Protein LigasesConceptsGlutamate receptor expressionPrefrontal cortexRepeated stressReceptor expressionRecognition memoryCognitive processesTemporal order recognition memoryPFC pyramidal neuronsStress-related mental disordersJuvenile male ratsGlutamatergic responsesGlutamatergic transmissionPyramidal neuronsMale ratsSynaptic transmissionStressed animalsInhibition of proteasomeMaladaptive changesGlucocorticoid receptorCognitive impairmentNR1 subunitMental disordersChronic stressUbiquitin/proteasome-mediated degradationReceptor turnoverDisrupted GABAAR trafficking and synaptic inhibition in a mouse model of Huntington's disease
Yuen EY, Wei J, Zhong P, Yan Z. Disrupted GABAAR trafficking and synaptic inhibition in a mouse model of Huntington's disease. Neurobiology Of Disease 2012, 46: 497-502. PMID: 22402331, PMCID: PMC3323696, DOI: 10.1016/j.nbd.2012.02.015.Peer-Reviewed Original ResearchConceptsHuntingtin associated protein 1Mouse modelHuntington's diseaseSynaptic inhibitionExcitatory/inhibitory balanceInhibitory synaptic efficacyDiminished surface expressionNeurodegenerative movement disorderTransgenic mouse modelHD mouse modelsNeuronal excitotoxicityInhibitory balanceMovement disordersAssociated protein 1Synaptic transmissionGABAAR traffickingSynaptic efficacySynaptic functionDiseaseReceptorsMutant huntingtinProtein 1Protein 5Surface expressionPolyglutamine repeats
2011
The Novel Antipsychotic Drug Lurasidone Enhances N-Methyl-d-aspartate Receptor-Mediated Synaptic Responses
Yuen EY, Li X, Wei J, Horiguchi M, Meltzer HY, Yan Z. The Novel Antipsychotic Drug Lurasidone Enhances N-Methyl-d-aspartate Receptor-Mediated Synaptic Responses. Molecular Pharmacology 2011, 81: 113-119. PMID: 22072817, PMCID: PMC3263951, DOI: 10.1124/mol.111.076141.Peer-Reviewed Original ResearchConceptsAtypical antipsychotic drugsEffect of lurasidoneSynaptic responsesVivo administrationN-methyl-D-aspartate (NMDA) receptor hypofunctionShort-term administrationCortical pyramidal neuronsAtypical APDsReceptor antagonist haloperidolAtypical APD clozapineKey molecular targetsSubchronic administrationPyramidal neuronsReceptor hypofunctionReceptor antagonismReceptor antagonistAntagonist haloperidolNMDAR responsesNMDAR synaptic functionAntipsychotic drugsNR2B subunitSerotonin 5Noncompetitive antagonistLurasidoneCognitive impairment