摘要目的:探讨肌醇对成年小鼠视皮层眼优势可塑性的再激活作用及其机制。方法:取出生后第60天(P60)雄性SPF级C57BL/6J小鼠32只，采用随机数字表法将其随机分为正常对照组、单眼形觉剥夺(MD)组、肌醇组(给予正常小鼠肌醇灌胃)和MD＋肌醇组(给予MD小鼠肌醇灌胃)，每组8只，其中MD组和MD＋肌醇组于P60行右眼MD。各组小鼠均饲养至P64，分别进行双眼图形视觉诱发电位(P-VEP)检查，测量P100波振幅和峰时，计算眼优势比值，即对侧同侧比(C/I)，评估眼优势转移情况。另取24只小鼠，采用随机数字表法将其随机分为MD组和MD＋肌醇组，每组12只，分别从2个组小鼠视皮层中提取RNA，进行转录组学测序和生物信息学分析，筛选差异表达基因。再取6只小鼠，采用随机数字表法将其随机分为MD组和MD＋肌醇组，每组3只，采用实时荧光定量PCR法检测差异表达基因细胞通信网络因子1( CCN1)、脂肪酸结合蛋白7( Fabp7)、半乳糖凝集素3结合蛋白( Lgals3bp)的表达变化。 结果:P-VEP结果显示，正常对照组、MD组、肌醇组和MD＋肌醇组右眼P100波振幅分别为(89.04±19.87)、(83.04±9.42)、(88.14±21.75)和(61.75±15.42)μV，P100波峰时分别为(102.40±5.64)、(101.50±8.26)、(101.33±8.66)和(111.30±7.17)ms，C/I分别为2.38±0.17、2.35±0.22、2.41±0.31和1.65±0.24，总体比较差异均有统计学意义( F＝5.844、2.221、16.634，均 P<0.05)，其中，与正常对照组、MD组和肌醇组相比，MD＋肌醇组右眼P100波振幅显著降低，P100波峰时显著延长，C/I显著降低，差异均有统计学意义(均 P<0.05)。正常对照组、MD组、肌醇组和MD＋肌醇组左眼P100波振幅和峰时总体比较差异均无统计学意义( F＝0.249、1.356，均 P>0.05)。转录组测序结果显示，MD＋肌醇组小鼠与MD组相比，有93个基因表达存在显著差异，其中与视觉可塑性相关的基因 CCN1、 Fabp7和 Lgals3bp的差异表达尤为显著。实时荧光定量PCR检测结果显示，MD＋肌醇组 CCN1表达显著降低， Fabp7和 Lgals3bp表达显著升高，差异均有统计学意义( t＝17.561、9.237、12.710，均 P<0.001)。 结论:肌醇能有效激活成年小鼠视皮层眼优势可塑性，并可能通过调节 CCN1、 Fabp7和 Lgals3bp等特定基因的表达介导这一过程。

abstractsObjective:To investigate the effect of myo-inositol on the reactivation of ocular dominance plasticity in the visual cortex of adult mice and its mechanisms.Methods:Thirty-two male SPF-grade C57BL/6J mice at postnatal day 60 (P60) were randomly divided into four groups using a random number table: normal control group, monocular form deprivation (MD) group, myo-inositol group (myo-inositol administered to normal mice), and MD+ myo-inositol group (myo-inositol administered to MD mice), with 8 mice in each group.The right eyes of MD group and MD+ myo-inositol group received MD on P60.Mice in each group were housed until P64 when pattern visual evoked potential (P-VEP) recordings were performed in both eyes.The amplitude and peak time of P100 wave were measured, and the contralateral/ipsilateral ratio (C/I) was calculated to evaluate the shift of ocular dominance.Twenty-four mice were randomly divided into MD group and MD+ myo-inositol group using the random number table method, with 12 mice in each group.RNA was extracted from the visual cortex of the two groups of mice, and transcriptomic sequencing and bioinformatics analysis were performed to screen differentially expressed genes.Six mice were randomly divided into MD group and MD+ myo-inositol group using the random number table method, with 3 mice in each group, and the expression changes of differentially expressed genes cell communication network factor 1( CCN1), fatty acid binding protein 7( Fabp7) and galectin-3 binding protein ( Lgals3bp) were verified by real-time fluorescence quantitative PCR.This study adhered to the Regulations on the Administration of Laboratory Animals (2017 Edition), and the research protocol was approved by the Animal Ethics Committee of Tianjin Medical University (No.TMUaMEC2022004). Results:The P-VEP results showed that the right eye P100 amplitudes in the normal control, MD, myo-inositol and MD+ myo-inositol groups were (89.04±19.87), (83.04±9.42), (88.14±21.75) and (61.75±15.42)μV, and the P100 wave peak time were (102.40±5.64), (101.50±8.26), (101.33±8.66) and (111.30±7.17)ms, and C/I were 2.38±0.17, 2.35±0.22, 2.41±0.31, and 1.65±0.24, respectively, with statistically significant overall differences ( F=5.844, 2.221, 16.634; all P<0.05).Compared with the normal control group, MD group and myo-inositol group, the MD+ myo-inositol group had a significant decrease in the P100 wave amplitude in the right eye, a significant prolongation of the P100 wave peak time, and a significant decrease in the C/I, with statistically significant differences (all P<0.05).There was no significant difference in P100 wave amplitude or peak time in the left eyes among the normal control, MD, myo-inositol and MD+ myo-inositol groups ( F=0.249, 1.356; both P>0.05).The transcriptome sequencing results showed that there were significant differences in the expression of 93 genes between the MD+ myo-inositol group and the MD group, among which the differential expression of CCN1, Fabp7 and Lgals3bp genes related to visual plasticity was particularly significant.The real-time fluorescence quantitative PCR results verified that the expression of CCN1 in the MD+ myo-inositol group was significantly decreased, and the expression of Fabp7 and Lgals3bp was significantly increased, with statistically significant differences ( t=17.561, 9.237, 12.710; all P<0.001). Conclusions:Myo-inositol can effectively reactivate ocular dominance plasticity in the visual cortex in adult mice, and may mediate this process by regulating the expression of specific genes CCN1, Fabp7, and Lgals3bp.