作者: Jose ´ RodrigoRodriguez
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摘要: Synapsesarespecializedcommunicationpointsbetweenneurons,andtheirnumberisamajordeterminantofcognitiveabilities.These dynamic structures undergo developmental- and activity-dependent changes. During brain aging certain diseases, synapses are gradually lost, causing mental decline. It is, thus, critical to identify the molecular mechanisms controlling synapse number. We show herethatthelevelsofphosphoinositide3kinase(PI3K)regulatesynapsenumberinbothDrosophilalarvalmotorneuronsandadultbrain projection neurons. The supernumerary induced by PI3K overexpression functional elicit changes in behavior. Remarkably,PI3Kactivationinducessynaptogenesisinagedadultneuronsaswell.WedemonstratethatpersistentPI3Kactivityisnecessary for maintenance. also report that controls expression localization of synaptic markers human neuroblastomacells,suggestingthatPI3Ksynaptogenicactivityisconservedinhumans.Thus,weproposethatPI3Kstimulationcanbeapplied topreventordelaysynapselossinnormalagingandinneurologicaldisorders.