〔Abstract〕 Objective To explore the effects of exposure to sevoflurane in neonatal mice on adolescent learning and memory and its related mechanisms. Methods 6-day-old C57 BL/6 mice were randomly divided into control group(CON group),sevoflurane group(SEVO group),control+lithium chloride group(LiCl group),sevoflurane+lithium chloride group(SEVO+LiCl group).The SEVO group was exposed to 3% sevoflurane for 3 consecutive days(day 6 to 8),once a day for 2 hours each time, the CON group was a 60% oxygen control, the LiCl group was intraperitoneally injected with GSK3β inhibitor lithium chloride(100 mg/kg) 30 minutes before 60% oxygen exposure, and the SEVO+LiCl group was given intraperitoneal injection of glycogen synthase kinase 3β(GSK3β) inhibitor lithium chloride(100 mg/kg) 30 minutes before exposure to sevoflurane.New object recognition experiment and Y maze experiment were used to detect the learning and memory ability of mice on day 30 to 32; Western blot was used to detect the content of myelin basic protein(MBP),β-catenin protein and the ratio of pGSK3β/GSK3β in mouse hippocampus. Results The results of behavioral experiments showed that the mouse Discrimination index and the percentage of novel arm in the SEVO group were lower than those in the CON group(P<0.05).After pretreatment with lithium chloride, the Discrimination index and the percentage of novel arm in the SEVO+LiCl group were higher than those in the SEVO group(P<0.05),and the learning and memory function was improved.Western blot results showed that the expressions of MBP protein, β-catenin protein and the ratio of pGSK3β/GSK3β in the hippocampus of the SEVO group were lower than those in the CON group(P<0.05).After pretreatment with lithium chloride, compared with the SEVO group, the expression of MBP protein and β-catenin protein in hippocampus of SEVO+LiCl group mice increased, and the ratio of pGSK3β/GSK3β increased(P<0.05). Conclusion Exposure to sevoflurane in neonatal mice causes impairment of learning and memory in adolescence, which may be related to the myelin damage of hippocampus caused by the inhibition of GSK3β/β-catenin signaling pathway GSK3β(Ser9) phosphorylation.