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目的:探讨丰富环境和贫瘠环境干预对锰中毒小鼠学习记忆能力和神经发生的影响。方法:成年昆明雌性小鼠40只,随机分成四组:空白对照组(对照组,CG)、正常环境染锰组(染锰组,SEG)、丰富环境干预染锰组(丰富组,EEG)、以及贫瘠环境干预染锰组(贫瘠组,IEG),每组10只。采用腹腔注射3周氯化锰(MnCl2 20mg/kg)的方式造模,Morris水迷宫检测小鼠学习记忆能力,免疫荧光法检测小鼠SVZ和SGZ内DCX的表达。结果:水迷宫定位航行试验染锰组小鼠的逃避潜伏期比对照组小鼠的明显延长(P<0.05),而丰富组小鼠的逃避潜伏期明显比染锰组小鼠的缩短(P<0.05),空间探索实验中,染锰组穿越平台的次数比对照组少,丰富组穿越平台的次数则比染锰组多,贫瘠组比染锰组少,差异有统计学意义(P<0.05)。染锰组和贫瘠组SVZ和SGZ区DCX阳性荧光强度明显比对照组弱,丰富组比染锰组强,差异均有统计学意义。结论:丰富环境可改善锰中毒小鼠的学习记忆能力,其机制可能与促进脑内神经发生有关。
Objective: To investigate the effects of rich environment and poor environmental intervention on learning and memory ability and neurogenesis in mice with manganese poisoning. Methods: Forty adult female Kunming mice were randomly divided into four groups: blank control group (CG), normal manganese group (S group) and enriched group (EEG) , And the poor environment intervention manganese group (infertile group, IEG), 10 in each group. The mice were injected intraperitoneally with MnCl2 (MnCl2 20mg / kg) for 3 weeks. The Morris water maze was used to detect the learning and memory ability of mice. The expression of DCX in SVZ and SGZ was detected by immunofluorescence. Results: The evacuation latency of the manganese-exposed group was significantly longer than that of the control group (P <0.05), while the escape latency of the enriched group was significantly shorter than that of the control group (P <0.05) ). In the space exploration experiment, the number of transglutaminase traversing platform was less than that of the control group, the number of enriching traversing platform was more than that of the manganese group, the less infertile group was less than that of the manganese group (P <0.05) . The positive fluorescence intensity of DCX in SVZ and SGZ of the Mn-deficient and Mn-deficient groups was significantly lower than that of the control group, and the enrichment group was stronger than that of the Mn-contaminated group. The difference was statistically significant. Conclusion: Enrichment environment can improve the learning and memory ability of mice with manganese poisoning, the mechanism may be related to the promotion of neurogenesis in the brain.