2022
Deficiency of transmembrane AMPA receptor regulatory protein γ-8 leads to attention-deficit hyperactivity disorder-like behavior in mice
Bai W, Luo X, Jin B, Zhu K, Guo W, Zhu X, Qin X, Yang Z, Zhao J, Chen S, Wang R, Hao J, Wang F, Shi Y, Kong D, Zhang W. Deficiency of transmembrane AMPA receptor regulatory protein γ-8 leads to attention-deficit hyperactivity disorder-like behavior in mice. 动物学研究 2022, 43: 851-870. PMID: 36031768, PMCID: PMC9486526, DOI: 10.24272/j.issn.2095-8137.2022.122.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAttention Deficit Disorder with HyperactivityCalcium ChannelsHumansMiceMice, KnockoutProteomicsConceptsAttention deficit hyperactivity disorderTARP γKO miceAttention deficit hyperactivity disorder-like behaviorsPrefrontal cortexDysregulation of dopaminergicDevelopment of ADHDGlutamate receptor complexAMPA receptor subunitsTransmembrane AMPA receptor regulatory protein (TARP) γADHD-like behaviorsADHD-like phenotypeMajor behavioral deficitsGlutamatergic transmissionHippocampal synaptosomesRisk factorsSchool-aged childrenAlternative animal modelBehavioral deficitsNew therapiesKnockout miceAnimal modelsProtein γMemory deficitsReceptor subunits
2016
Glutamate carboxypeptidase II gene knockout attenuates oxidative stress and cortical apoptosis after traumatic brain injury
Cao Y, Gao Y, Xu S, Bao J, Lin Y, Luo X, Wang Y, Luo Q, Jiang J, Neale JH, Zhong C. Glutamate carboxypeptidase II gene knockout attenuates oxidative stress and cortical apoptosis after traumatic brain injury. BMC Neuroscience 2016, 17: 15. PMID: 27091009, PMCID: PMC4836105, DOI: 10.1186/s12868-016-0251-1.Peer-Reviewed Original ResearchConceptsTraumatic brain injuryWild-type miceBrain injuryKnockout miceNeuroprotective efficacyType miceImpact injuryOxidative stressCortical impact injuryInjury-induced increaseBcl-2/Bax ratioGene knockout miceGlutathione peroxidase activityCerebral cortexCortical apoptosisKO miceCytosolic cytochrome c levelsConclusionsThese dataN-acetylaspartylglutamateSynaptic releaseTUNEL-positive nucleiAnimal modelsExtracellular levelsCytochrome c levelsGlutathione levels
2015
Mice lacking glutamate carboxypeptidase II develop normally, but are less susceptible to traumatic brain injury
Gao Y, Xu S, Cui Z, Zhang M, Lin Y, Cai L, Wang Z, Luo X, Zheng Y, Wang Y, Luo Q, Jiang J, Neale JH, Zhong C. Mice lacking glutamate carboxypeptidase II develop normally, but are less susceptible to traumatic brain injury. Journal Of Neurochemistry 2015, 134: 340-353. PMID: 25872793, DOI: 10.1111/jnc.13123.Peer-Reviewed Original ResearchConceptsTraumatic brain injuryGlutamate carboxypeptidase IIModerate traumatic brain injuryNeurotransmitter N-acetylaspartylglutamateGCPII geneBrain injuryNervous systemSpatial learning/memoryEnhanced glutamate transmissionLong-term behavioral outcomesHippocampus 24 hInhibition of GCPIIWild-type littermatesMorris water mazeCarboxypeptidase IIKO mouse lineLearning/memoryHistopathological protectionGene KOBeam walkingGlutamate transmissionNeuronal degenerationAstrocyte damageKO miceNeurological behavior