{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,7]],"date-time":"2026-08-07T15:18:47Z","timestamp":1786115927917,"version":"build-2736575974"},"reference-count":32,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2026,6,29]],"date-time":"2026-06-29T00:00:00Z","timestamp":1782691200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,6,29]],"date-time":"2026-06-29T00:00:00Z","timestamp":1782691200000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Synapse"],"published-print":{"date-parts":[[2026,7]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>This study aimed to investigate the role and underlying mechanism of lncRNA MIAT in sevoflurane (Sev)\u2010induced cognitive dysfunction in neonatal rats, thereby offering theoretical basis for clinical intervention. Seven\u2010day\u2010old Sprague\u2010Dawley (SD) rats were chosen to construct a Sev\u2010induced cognitive dysfunction model. Anxiety\u2010like behavior and locomotor activity were assessed by the open field test (OFT), whereas cognitive function was evaluated using novel object recognition (NOR) test and Morris water maze (MWM) test. The expression levels of lncRNA MIAT, miR\u201015b\u20105p, and Ccnd1 were detected by RT\u2010qPCR. The dual\u2010luciferase reporter gene assay was carried out to validate the targeted binding relationships. Sev exposure led to a downregulation of lncRNA MIAT expression in rat hippocampus. lncRNA MIAT alleviated Sev\u2010induced cognitive impairment, as manifested by increased central zone residence time in OFT, elevated recognition index (RI) in NOR test, shortened escape latency, increased platform crossings, and prolonged target quadrant residence time in MWM test. Mechanistically, lncRNA MIAT directly targeted miR\u201015b\u20105p and inhibited its expression. miR\u201015b\u20105p targeted Ccnd1 and suppressed its expression. Overexpression of miR\u201015b\u20105p or silencing of Ccnd1 reversed the neuroprotective effect of lncRNA MIAT. LncRNA MIAT ameliorates Sev\u2010induced cognitive dysfunction in neonatal rats by sponging miR\u201015b\u20105p to upregulate Ccnd1 expression, which may serve as a potential target for preventing Sev\u2010related neurotoxicity.<\/jats:p>","DOI":"10.1002\/syn.70050","type":"journal-article","created":{"date-parts":[[2026,6,30]],"date-time":"2026-06-30T04:00:00Z","timestamp":1782792000000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["LncRNA MIAT Protects Against Sevoflurane\u2010Induced Cognitive Dysfunction in Neonatal Rats via the miR\u201015b\u20105p\/Ccnd1 Axis"],"prefix":"10.1002","volume":"80","author":[{"given":"Xuewen","family":"Lu","sequence":"first","affiliation":[{"name":"Anesthesiology Department Zhongda Hospital (Jiangbei) Southeast University  Nanjing Jiangsu 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