运动对脑老化小鼠学习记忆能力及突触可塑性的影响

目的从突触可塑性方面探讨运动的抗脑老化作用及其机制。方法雄性ICR小鼠40只分为4组,即脑老化模型组、脑老化+运动组、运动对照组、普通对照组,每组10只。以电动跑台进行有氧跑步运动,速度25m/min,持续运动20min,每天运动1次,每周运动6d,休息1d。以D-半乳糖100mg/kg·d颈背部皮下注射制备脑老化模型。实验干预期共9周。以Morris水迷宫测试小鼠空间记忆和学习能力,流式细胞术测定皮层海马神经元突触体数量,荧光偏振法测定突触体膜流动性,羟胺比色法测定脑组织乙酰胆碱酯酶(AChE)活性。结果(1)水迷宫实验中,脑老化组小鼠的逃避潜伏期(EL)明显大于普通对照组小鼠(P<0.05),脑老化+运动组小鼠的EL低于脑老化组(P<0.05)而与普通对照组无显著差异,运动对照组与普通对照组小鼠的EL无显著差异(P>0.05)。(2)脑老化组和脑老化+运动组小鼠突触体数量低于非脑老化组(运动对照组和普通对照组,P<0.05),脑老化+运动组高于脑老化组(P<0.05),运动对照组与普通对照组无显著差异(P>0.05)。(3)突触体膜流动性:脑老化组小鼠突触体膜粘滞度高于非脑老化组并且高于脑老化+运动组(P<0.05),脑老化运动组与非脑老化组之间、运动对照组与普通对照组之间无显著差异(P>0.05)。(4)脑老化组和脑老化+运动组小鼠脑组织AchE活性高于非脑老化组(P<0.05),运动对照组与普通对照组之间无显著差异(P>0.05)。结论运动能够减轻脑老化小鼠空间学习记忆能力的衰退。

Effects of exercise on spatial learning and hippocampal synaptic plasticity in brain aging mice

Objective To examine the effects and mechanism of exercise on resisting brain aging from the aspect of synaptic plasticity. Methods Forty male ICR mice were randomly divided into 4 groups: the D-galactose- induced brain aging,brain aging plus exercise,exercise only and normal controls. Mice were subjected to treadmill running at intensity (25m /min for 20min daily,6 days a week) level of exercise and were given 100mg·kg -1·d -1 subcutaneous injection of D-galactose to prepare brain aging model for 9 weeks. The Morris water maze (MWM) test was employed to determine their spatial learning and memory ability. Flow cytometry (FCM) was used to analyze the amount of hppocampal synaptosomes. Membrane fluidity of synaptosomes was measured by fluorescence polarization technique. Acetylcholinesterase ( AChE ) activity in brain was determined by hydroxylaminecolorimetric assay. Results (1)In Morris water maze test,brain aging mice showed a significant longer escape latency (EL) than the normal control mice (P < 0. 05). Brain aging mice plus exercise exhibited a significant shorter EL than brain aging mice (P < 0. 05),but no difference was found when compared with normal control mice (P > 0. 05). There were no statistical difference in EL between the controls and exercise group (P > 0. 05). (2)The number of synaptosomes in brain aging mice and brain aging mice plus exercise were less than those in non-brain aging mice (the exercise and the control mice) (P < 0. 05). The number of synaptosomes in brain aging mice plus exercise was more than brain aging mice (P < 0. 05). There were no statistical difference in the number of synaptosomes between the controls and exercise group (P > 0. 05). (3)Membrane fluidity of synaptosomes: the viscosity of membrane in brain aging group was higher than in non-brain aging group,and higher than brain aging plus exercise group (P < 0. 05). There wereno statistical difference in viscosity of membrane between brain aging group and non-brain aging group,and between the controls and exercise group (P > 0. 05). (4) The AChE activity in brain aging and brain aging plus exercise group were higher than those in control and exercise group (P < 0. 05). There were no statistical difference in AChE activity between the controls and exercise group ( P > 0. 05). Conclusion Exercise can effectively protect against decline in the capacity of learning and memory in brain aging mice.