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Proteomic analysis, RNA immunoprecipitation, and real-time qPCR identified GABA\n                    <jats:sub>B<\/jats:sub>\n                    R1 as a key downstream target of NAT10.\n                    <jats:italic>Nat10<\/jats:italic>\n                    deletion reduced GABA\n                    <jats:sub>B<\/jats:sub>\n                    R1 expression, and subsequently weakened inhibitory postsynaptic currents in hippocampal DG neurons. Further analysis revealed that microglia activation and the release of inflammatory mediators lead to the increased NAT10 expression in neurons. Microglia depletion with PLX3397 effectively reduced NAT10 and GABA\n                    <jats:sub>B<\/jats:sub>\n                    R1 expression in neurons, and ameliorated cognitive dysfunction induced by SAE. In summary, our findings revealed that after CLP, NAT10 in hippocampal DG neurons promotes GABA\n                    <jats:sub>B<\/jats:sub>\n                    R1 expression through mRNA acetylation, leading to cognitive dysfunction.\n                  <\/jats:p>","DOI":"10.1073\/pnas.2410564121","type":"journal-article","created":{"date-parts":[[2024,8,27]],"date-time":"2024-08-27T11:38:01Z","timestamp":1724758681000},"update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":32,"title":["N-acetyltransferase 10 mediates cognitive dysfunction through the acetylation of GABA\n                    <sub>B<\/sub>\n                    R1 mRNA in sepsis-associated encephalopathy"],"prefix":"10.1073","volume":"121","author":[{"given":"Shenjia","family":"Gao","sequence":"first","affiliation":[{"name":"Department of Anesthesiology, Zhongshan Hospital, Fudan University, Shanghai 200032, China"},{"name":"Shanghai Key Laboratory of Perioperative Stress 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