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作者（2019）在《Endothelium-Derived Semaphorin 3G Regulates Cognitive Function》一文中研究指出：Objective:The proper interactions between blood vessels and neurons are critical for maintaining the strength of neural circuits and cognitive function. However,the precise molecular events underlying these interactions remain largely unknown. Semaphorin 3 G（Sema3 G） is expressed mainly in endothelial cells,not in neuronal or glial cells in the brain. Here,we want to explore whether and how vascular-derived semaphorin 3 G regulate synaptic structure and plasticity of pyramidal neurons at CA1. Methods:Using biochemistry and transcriptional profiling analysis,to find Sema3 G is expressed almost exclusively in ECs in the brain;To study the function of EC-derived Sema3 G,we generated endothelial Sema3 G conditional-knockout mouse(Cdh5-Cre;Sema3 Gf/f);Through electrophysiology,optogenetic strategies and behavior analysis,to examine endothelial Sema3 G losing lead to learning and memory defects,and synaptic plasticity at CA1 in mice;Finally,The re-expressing Sema3 G in the hippocampus could reverse the defects of spine density loss and cognitive dysfunction observed in Cdh5-Cre;Sema3 Gf/f mice. Results:our data showed that the selective knockout of semaphorin 3 G in endothelial cells impaired hippocampal-dependent memory and reduced dendritic spine density in CA1 neurons in mice;these effects were reversed after restoration of Sema3 G levels in the hippocampus by AAV transfection. We further show that Sema3 G increased excitatory synapse density via neuropilin-2/PlexinA4 signaling and through activation of Rac1. Conclusion:These results provide the first evidence that,in the central nervous system,endothelial Sema3 G serves as a vascular-derived synaptic organizer that regulates synaptic plasticity and hippocampal-dependent memory. Our findings highlight the role of vascular endothelial cells in regulating cognitive function through intercellular communication with neurons in the hippocampus.
Abstract
Objective:The proper interactions between blood vessels and neurons are critical for maintaining the strength of neural circuits and cognitive function. However,the precise molecular events underlying these interactions remain largely unknown. Semaphorin 3 G（Sema3 G） is expressed mainly in endothelial cells,not in neuronal or glial cells in the brain. Here,we want to explore whether and how vascular-derived semaphorin 3 G regulate synaptic structure and plasticity of pyramidal neurons at CA1. Methods:Using biochemistry and transcriptional profiling analysis,to find Sema3 G is expressed almost exclusively in ECs in the brain;To study the function of EC-derived Sema3 G,we generated endothelial Sema3 G conditional-knockout mouse(Cdh5-Cre;Sema3 Gf/f);Through electrophysiology,optogenetic strategies and behavior analysis,to examine endothelial Sema3 G losing lead to learning and memory defects,and synaptic plasticity at CA1 in mice;Finally,The re-expressing Sema3 G in the hippocampus could reverse the defects of spine density loss and cognitive dysfunction observed in Cdh5-Cre;Sema3 Gf/f mice. Results:our data showed that the selective knockout of semaphorin 3 G in endothelial cells impaired hippocampal-dependent memory and reduced dendritic spine density in CA1 neurons in mice;these effects were reversed after restoration of Sema3 G levels in the hippocampus by AAV transfection. We further show that Sema3 G increased excitatory synapse density via neuropilin-2/PlexinA4 signaling and through activation of Rac1. Conclusion:These results provide the first evidence that,in the central nervous system,endothelial Sema3 G serves as a vascular-derived synaptic organizer that regulates synaptic plasticity and hippocampal-dependent memory. Our findings highlight the role of vascular endothelial cells in regulating cognitive function through intercellular communication with neurons in the hippocampus.
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