跑台训练对阿尔茨海默病模型大鼠记忆能力和突触可塑性的影响

关键词：阿尔茨海默病  运动  脑源性神经营养因子  突触可塑性

Keywords:Alzheimer's disease  exercise  brain derived neurotrophic factor  synaptic plasticity

摘要：

      摘要 目的：观察8周跑台运动对阿尔茨海默病模型大鼠记忆能力和突触可塑性的影响及内在机制。 方法：60只雄性SD大鼠随机分为正常对照组（NC组）、AD模型对照组（AC组）、AD模型训练组（AE组）。通过向大鼠两侧海马区注射Aβ25-35制造AD模型，Morris水迷宫实验检测各组大鼠记忆能力，Golgi法检测海马神经元树突密度；Western blot法检测海马组织中BDNF、SYP、PSD-95、P-Akt、P-CREB的表达。 结果：与AC组比较，AE组大鼠逃避潜伏期明显减少，穿越平台区域次数明显增加（P＜0.01）；Golgi染色结果表明，AE组海马神经元侧树突密度明显增加（P＜0.01）；Western blot检测结果表明，与AC组相比，AE组BDNF、SYP、PSD-95、P-Akt表达都明显增强（P＜0.01），但P-CREB表达无显著性变化（P＞0.05）。 结论：8周跑台训练可增加AD模型大鼠海马组织BDNF、SYP、PSD-95、P-Akt的蛋白表达，可能与海马神经元树突密度增加有关，或许是AD模型大鼠的记忆能力改善和突触可塑性变化的基础。

Abstract:

      Abstract Objective: To observe the effect of treadmill exercise for 8 weeks on memory and synaptic plasticity in rat model with Alzheimer's disease（AD） and internal mechanism. Method: Sixty male SD rats were randomly divided into normal control group (NC), Alzheimer Control Group (AC), Alzheimer Exercise Group (AE). AD model was made by bilateral hippocampal injection of A beta 25-35. Morris water maze was used to detect the learning and memory ability of rats in each group. Golgi method was used to detect the density of dendritic in hippocampal neurons. Western blot method was used to detect the expression of BDNF, SYP, PSD-95, P-Akt and P-CREB in hippocampus. Result: Compared with AC group, AE group showed obviously decreased escape latency with a significant increase in the number of crossing the platform area (P＜0.01). Golgi staining results showed that the dendritic density in hippocampal neuron of AE group increased significantly (P＜0.01). Western blot testing results showed that the expression of BDNF, SYP, PSD-95 and P-Akt in AE group were significantly enhanced,when compared with AC group, (P＜0.01). However, the expression of P-CREB had no significant change (P＞0.05). Conclusion: Eight weeks of treadmill exercise can increase the expression of BDNF, SYP, PSD-95 and P-Akt protein in the hippocampus of AD model rats, which cause an increase in dendritic density, thereby improving the memory and synaptic plasticity in rat model with AD.