{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Andoh M"],"funding":["MEXT | Japan Society for the Promotion of Science","MEXT | Japan Society for the Promotion of Science (JSPS)","Japan Agency for Medical Research and Development","MEXT | JST | Exploratory Research for Advanced Technology","MEXT | JST | Exploratory Research for Advanced Technology (ERATO)","Japan Agency for Medical Research and Development (AMED)"],"pagination":["918"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11754728"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["16(1)"],"pubmed_abstract":["Caspases are known to mediate neuronal apoptosis during brain development. However, here we show that nonapoptotic activation of caspase-3 at presynapses drives microglial synaptic phagocytosis. Real-time observation and spatiotemporal manipulation of synaptic caspase-3 in the newly established, mouse-derived culture system demonstrate that increased neuronal activity triggers localized presynaptic caspase-3 activation, facilitating synaptic tagging by complements. High-resolution live imaging reveals that caspase-3 activation promotes synapse-selective complement-dependent microglial phagocytosis without axonal shearing. Furthermore, activity-dependent caspase-3 activation at inhibitory presynapses induces microglial phagocytosis in mice and increases seizure susceptibility. This increase"],"journal":["Nature communications"],"pubmed_title":["Nonapoptotic caspase-3 guides C1q-dependent synaptic phagocytosis by microglia."],"pmcid":["PMC11754728"],"funding_grant_id":["23836218","21H04774","24H00567","JPMJER1801","20H05897","23H04766"],"pubmed_authors":["Andoh M","Koyama R","Araki T","Miura M","Ikegaya Y","Shinoda N","Taira Y","Takeuchi H","Kasahara Y"],"additional_accession":[]},"is_claimable":false,"name":"Nonapoptotic caspase-3 guides C1q-dependent synaptic phagocytosis by microglia.","description":"Caspases are known to mediate neuronal apoptosis during brain development. However, here we show that nonapoptotic activation of caspase-3 at presynapses drives microglial synaptic phagocytosis. Real-time observation and spatiotemporal manipulation of synaptic caspase-3 in the newly established, mouse-derived culture system demonstrate that increased neuronal activity triggers localized presynaptic caspase-3 activation, facilitating synaptic tagging by complements. High-resolution live imaging reveals that caspase-3 activation promotes synapse-selective complement-dependent microglial phagocytosis without axonal shearing. Furthermore, activity-dependent caspase-3 activation at inhibitory presynapses induces microglial phagocytosis in mice and increases seizure susceptibility. This increase","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Jan","modification":"2025-04-18T14:26:59.963Z","creation":"2025-04-07T00:36:08.264Z"},"accession":"S-EPMC11754728","cross_references":{"pubmed":["39843445"],"doi":["10.1038/s41467-025-56342-7"]}}