目的：检测敏感期内单眼形觉剥夺大鼠应用左旋多巴后视皮质中NNMDAR1的表达情况并与对照组对比，探讨左旋多巴改善视功能的作用部位及其分子机制。

方法：选取60只2周龄健康SD大鼠随机分为4组，正常组15只，另外45只行单侧眼睑缝合制作单眼形觉剥夺动物模型，制模成功后随机分为单眼形觉剥夺组(MD组)，生理盐水组(NS组)，左旋多巴组(LD组)，每组各15只。各组大鼠均在正常日光照射条件下饲养至45日龄。处死MD组及正常组大鼠，分别用免疫组化，蛋白免疫印记，实时荧光定量PCR的方法检测这两组大鼠视皮质中NMDAR1的表达情况。LD组和NS组在46日龄时分别给予左旋多巴(40mg/kg)和生理盐水灌胃，连续28d，分别用前述方法检测视皮质中NMDAR1的表达。

结果：MD组大鼠视皮质中NMDAR1的蛋白及mRNA表达均低于对照组； LD组大鼠视皮质中NMDAR1的蛋白及mRNA表达均高于NS组。

结论：NMDAR1与视觉发育的可塑性有关，左旋多巴能够逆转因形觉剥夺引起的NMDAR1表达下降。这一机制可能与其能够改善视功能的作用有关，其作用部位可能在于视皮质。

AIM: To detect expression of N-methyl-D-aspartate receptor-1-subunit(NMDAR1)in visual cortex of monocular deprivation rats during sensitive period and compare with that of normal group, to explore the site of NMDAR1 action in improving visual acuity and its molecular mechanism.

METHODS: Sixty 14-day-old healthy SD rats were randomly divided into 4 groups including normal group, monocular deprivation(MD)group, normal saline(NS)group, levodopa(LD)group, 15 rats for each. All the rats except those in the normal group were performed monocular deprivation surgery to establish monocular deprivation animal models and were raised in normal sunlight to 45-day-old. Rats in the MD group and normal group were killed and then marked by immunohistochemical and immune protein printing, respectively. The expression of NMDAR1 in visual cortex of these two groups were measured by quantitative real time PCR method. LD and NS groups were administered with levodopa(40mg/kg)and normal saline for 28d. The expression of NMDAR1 was examined with the same method.

RESULTS:NMDAR1 expression in visual cortex of MD group was lower than that in normal group. NMDAR1 expression in visual cortex of LD group was higher than that in NS group.

CONCLUSION: NMDAR1 is associated with the plasticity of visual development. Levodopa may revert the reduction of expression of NMDAR1 caused by monocular deprivation. This mechanism may be related with NMDAR1 capacity of improving visual function whose site of action may lie in the parts of the visual cortex.