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目的:研究慢性酒精摄入对小脑分子层感觉信息传递的影响，揭示慢性酒精中毒对小脑皮质感觉信息传递与信息整合影响的机制。方法:50只6～8周龄健康雄性ICR小鼠按照随机数字表法分为生理盐水组(对照组)和酒精摄入组(酒精组)，每组25只，酒精组每日腹腔注射体积分数为20%酒精，对照组则注射同等剂量的生理盐水，所有小鼠每天腹腔注射一次，连续注射28 d。通过电生理技术运用膜片钳放大器及数据采集软件记录感觉刺激诱发酒精组及对照组小鼠小脑分子层场电位变化。采用Clampfit 10.3软件对电生理数据进行记录分析，采用SPSS 22.0软件对数据进行统计分析，使用配对n t检验和单因素方差分析比较用药前后的差异。n 结果:给予吹风刺激后，酒精组小鼠的P1振幅较对照组显著增高[(121.3±3.5)%，(97.2±2.7)% ；n t＝26.08，n P0.05)及洗脱后(102.5±4.5)%(n t＝1.92，n P>0.05)比较，均差异无统计学意义；P1曲线下面积(103.5±2.6)%较给药后(102.5±4.6)%(n t＝0.99，n P>0.05)及洗脱后(101.9±3.7)%(n t＝1.81，n P>0.05)差异无统计学意义。对照组小鼠脑表面灌流一氧化氮供体SNAP后，吹风刺激诱发分子层场电位P1振幅(128.2±3.4)%较给药前(103.5±2.6)%显著增加(n t＝28.89，n P0.05)，P1曲线下面积(125.4±4.4)%较给药前(104.3±4.6)%显著增加(n t＝16.60，n P0.05)。n 结论:慢性酒精摄入显著增强抑制性反应，抑制性成分的增强源于NO信号通路的激活。“,”Objective:To investigate the effect of chronic ethanol consumption on sensory information transmission in the cerebellar molecular layer and reveal the mechanism of chronic alcoholism on sensory information transmission and integration in the cerebellar cortex.Methods:Fifty healthy male ICR mice aged 6-8 weeks were randomly divided into saline group(control group)and ethanol consumption group(alcohol group) according to the random number table, with 25 mice in each group.The mice in alcohol group were injected intraperitoneally with 20% ethanol daily, while the mice in control group were injected with the same dose of normal saline. All mice were injected intraperitoneally once a day for 28 days.Through electrophysiological technology, patch-clamp amplifier and data acquisition software were used to record the changes in cerebellar molecular layer field potential of mice in the alcohol group and control group induced by sensory stimulation.Clampfit 10.3 software was used to record and analyze the electrophysiological data. SPSS 22.0 software was used for statistical analysis. Paired n t-test and one-way ANOVA were used to analyze the differences before and after treatment.n Results:After giving the stimulation of wind blowing, the amplitude of P1 in alcohol group was significantly higher than that in control group ((121.31±3.5)%, (97.2±2.7)%; n t=26.08, n P0.05) and after elution(102.5±4.5)%,n t=1.92, n P>0.05). And the AUC of P1 in control group after perfused L-NNA had no differences compared with before administration(103.5±2.6)%, (102.5±4.6)%) and after elution((101.9±3.7)%,n t=0.99, 1.81, both n P>0.05). When the mouse brain surface was perfused with NO donor SNAP, the amplitude of P1 in the control group was significantly higher than that before administration( (128.2±3.4)%, (103.5±2.6)%;n t=28.89, n P0.05). The AUC of P1((125.4±4.4)%) was higher than before administration((104.3±4.6)% ,n t=16.60, n P0.05).n Conclusion:Chronic ethanol consumption significantly enhances the inhibitory response, and the enhancement of inhibitory components stems from the activation of the NO signaling pathway.