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MDGA2 Constrains Glutamatergic Inputs Selectively onto ca1 pyramidal neurons to Optimize Neural Circuits for Plasticity,Memory,and Social Behavior

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Neuroscience Bulletin 2024年第7期40卷 887-904页

作者： Xuehui Wang Donghui Lin Jie Jiang Yuhua Liu Xinyan Dong Jianchen Fan Lifen Gong Weida Shen Linghui Zeng Tonghui Xu Kewen Jiang Steven A.Connor Yicheng Xie School of Life Sciences Nanchang UniversityNanchang330031China Department of Neurology Children's HospitalZhejiang University School of MedicineNational Clinical Research Center for Child HealthHangzhou 310052China Department of Biology York University4700 Keele StreetTorontoON M3J 1P3Canada Key Laboratory of Novel Targets and Drug Study for Neural Repair of Zhejiang Province School of MedicineHangzhou City UniversityHangzhou 310015China

Synapse organizers are essential for the development,transmission,and plasticity of *** as rare synapse suppressors,the MAM domain containing glycosylphosphatidylinositol anchor(MDGA)proteins contributes to synapse organization by inhibiting the formation of the synaptogenic neuroligin-neurexin complex.A previous analysis of MDGA2 mice lacking a single copy of Mdga2 revealed upregulated glutamatergic synapses and behaviors consistent with ***,MDGA2 is expressed in diverse cell types and is localized to both excitatory and inhibitory *** the network versus cell-specific effects of MDGA2 loss-of-function requires a cell-type and brain region-selective *** address this,we generated mice harboring a conditional knockout of Mdga2 restricted to ca1 pyramidal *** we report that MDGA2 suppresses the density and function of excitatory synapses selectively on pyramidal neurons in the mature *** deletion of Mdga2 in ca1 pyramidal neurons of adult mice upregulated miniature and spontaneous excitatory postsynaptic potentials,vesicular glutamate transporter 1 intensity,and neuronal *** effects were limited to glutamatergic synapses as no changes were detected in miniature and spontaneous inhibitory postsynaptic potential properties or vesicular GABA transporter ***,evoked basal synaptic transmission and AMPAR receptor currents were enhanced at glutamatergic *** a behavioral level,memory appeared to be compromised in Mdga2 cKO mice as both novel object recognition and contextual fear conditioning performance were impaired,consistent with deficits in long-term potentiation in the ca3-ca1 *** affiliation,a behavioral analog of social deficits in autism,was similarly *** results demonstrate that MDGA2 confines the properties of excitatory synapses to ca1 neurons in mature hippocampal circuits,thereby optimizing this network for plasticity,c

关键词： MDGA2 ca1 pyramidal neurons Glutamatergic inputs Synaptic plasticity Memory Social behaviors Autism Synapse organizers

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