摘要
目的探讨脑发育不同阶段丰富环境(EE)刺激对缺氧缺血性脑损伤(HIBD)新生鼠神经可塑性的影响及机制。方法7日龄SD大鼠通过结扎左侧颈总动脉,吸入8%氧氮混合气,制成HIBD模型,分为早期干预组、晚期干预组、非干预组,另设假手术组。早期干预组于脑发育关键期内,即建模后第2天开始进行EE干预。晚期干预组于脑发育关键期后,即建模后第23天(日龄30d)开始进行EE干预。两组干预条件一致,总干预时间为20d。各组大鼠饲养至日龄100d时用免疫组织化学法检测患侧海马微管相关蛋白-2(MAP-2)的表达水平。结果早期干预组患侧海马MAP-2的表达明显高于晚期干预组和非干预组(P<0.01),早期干预组与假手术组差异无统计学意义(P>0.05),晚期干预组MAP-2的表达高于非干预组(P<0.05)。结论EE干预可增强神经可塑性。MAP-2在海马表达的变化,可能参与了脑发育不同阶段EE对HIBD神经可塑性的影响机制。
Objective To explore the effects of environmental stimulation on neuronal plasticity and possible mechanisms at diferent stages of development of hypoxiaqschemic brain damaged(HIBD) postnatal rats. Methods The Sprague Dawley(SD) rats' models of HIBD were established by the method of Rice. Then the rats with HIBI) were divided randomly into 3 groups:early intervention group,late intervention group and non-intervention group. The sham-operation rats served as sham-operation group. Environmental enrichment intervention was administrated to the early intervention group rats for 20d since 2d after HIBD. The same intervention to the late intervention group rats since 23d after HIBD. On the age of 100d. the immunohistochemieal stain was used to detect the gray values of MAP-2 in hippocampus respectively. Results Immunhistochemical analysis showed that the expression of MAP-2 in left-sided hippocampus of early intervention group significantly increased as compared with that of late intervention group (P〈0. 01). There was no significant difference between early intervention group and sham group(P〉0.05) ,and the expression of MAP-2 of late intervention group were stronger than that of non-intervention group (P〈0.05). Conclusion The neuronal plasticity of early intervention group is promoted more than that of late intervention group. The changes of MAP-2 in their hippocampuses are possibly associated with the influence of environment on neuronal plasticity at different developmental stage of HIBD.
出处
《重庆医学》
CAS
CSCD
北大核心
2009年第22期2790-2792,共3页
Chongqing medicine
关键词
缺氧缺血性脑损伤
丰富环境
发育脑
关键期
神经可塑性
微管相关蛋白
hypoxia-ischemic brain damage
environmental enrichment
developmental brain
critical period
neuronal plasticy
Microtube-associated protein-2