目的:建立小鼠长期酒精注射中毒模型，探讨长期酒精摄入对小鼠小脑皮层苔藓纤维-颗粒细胞感觉信息突触传递的影响机制。方法:20只6～8周龄的健康雄性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10只。酒精摄入组每日腹腔注射浓度为20%的酒精，对照组则注射同等剂量的生理盐水，注射周期均为28 d。注射结束后，在小脑的Crus Ⅱ区清除头皮及肌肉组织，去除颅骨，剥离硬脑膜，利用气体喷射装置在同侧触须垫30 mm处给予吹风刺激，寻找最大反应部位后，在小鼠脑表面灌流NMDA受体阻断剂[D-(-)-2-amino-5-phosphono-valerate，D-APV]、代谢性谷氨酸受体1阻断剂(JNJ16259685)及N-甲基-D-天冬氨酸(N-Methyl-D-aspartic acid，NMDA)，每种药物灌流20 min，两种药物之间用人工脑脊液充分灌流直到波形恢复，期间通过膜片钳技术，记录小鼠小脑颗粒层电位波形的变化特点。采用Clampfit 10.3软件和SPSS 22.0软件对所有实验数据进行统计分析。结果:给予吹风刺激后酒精组小鼠颗粒层场电位反应的潜伏期(11.8±0.7)ms较对照组(10.1±0.2)ms显著延长(n t＝-8.041，n P0.05)。酒精组小鼠脑表面灌流D-APV后，吹风刺激诱发的场电位P1的振幅[(42.3±1.5)mV]较给药前[(101.1±0.9)mV]及洗脱后[(100.1±2.2)mV]均显著降低(n t＝106.762，-69.605；均n P0.05). When D-APV was perfused into the brain surface of mice in the alcohol group, the amplitude of P1 ((42.3±1.5) Mv)was significantly lower than that before administration ((101.1±0.9)mV) and after elution ((100.1±2.2) mV) (n t=106.762, - 69.605, both n P<0.05), and the area under waveform of P1 ((42.6±1.3)%) was also significantly lower than that before administration ((100.6±1.6)%) and after elution ((97.6±2.2)%) (n t=88.862, -67.791, both n P<0.05).The ratio of N2 / N1 (0.3±0.1) was significantly lower than that before administration (0.4±0.1) and after elution (0.3±0.1) (n t=2.242, 2.121, both n P<0.05). When NMDA was perfused on the brain surface of mice in the control group, compared with before administration and after elution, the amplitude of P1 ((110.7±3.2) mV, (100.1±0.9) mV, (102.0±1.7) mV,n t=-10.173, 7.669, both n P<0.05), the area under the waveform of P1 ((127.9±3.5)%, (100.0±3.1)%, (115.0±5.3)%,n t=-18.698, 6.447, both n P<0.05), the ratio of N2 / N1 ((0.5±0.1), (0.3±0.1), (0.3±0.1),n t=-5.669, 5.669, both n P0.05).n Conclusion:Long-term alcohol intake significantly suppresses the synaptic transmission of excitatory glutamate in MF-GC, and enhances the inhibitory response mediated by GABAA receptor in cerebellar cortex. The inhibitory component is enhanced by NMDA receptor, but not by type 1 metabolic glutamate receptor.