反复力竭游泳运动对小鼠前脑皮层和海马的影响

摘要

Acute stress and chronic stress can damage the brain prefrontal cortex( PFC)and hippo-campus( HP)function,then reduce learning and memory abilities of animal or human. Model of exhaustive exercise mice was set up by the way of repeatedly( four weeks)exhausted swimming. Membrane fluidity and free calcium concentrations([ Ca2+]i)of prefrontal cortical and hippocam-pal synaptosomes in mice were detected. The results show that,compared with control group mice, the membrane fluidity of synaptosomes in PFC and HP of exhaustive exercise group mice were signif-icantly decreased at 0 h and 12 h,after repeatedly exhausted exercise. The synaptosomal[ Ca2+]i in PFC and HP were significantly increased at 0 h,12 h and 24 h in exhaustive exercise group mice. The[ Ca2+]i in PFC and HP at 1 week were remarkably reduced than the exhaustive exercise 0 h group mice,respectively. The generation and recovery of exercise-induced central fatigue in mice after exhausted exercise which may be nearly related to the changes of membrane fluidity and [ Ca2+]i of synaptosomes.%急性应激和长期慢性应激均可损伤脑内的海马和前额叶，继而降低动物或人的学习记忆能力。采用4周反复力竭游泳运动方式建立力竭运动小鼠模型。在反复性力竭游泳运动后即刻（0 h）、12 h、24 h和1周，检测小鼠前脑皮层和海马突触体膜流动性变化，以及突触体内游离Ca2+浓度。结果表明，反复性力竭游泳运动后，与对照组小鼠比较，力竭运动组小鼠前脑皮层和海马突触体膜流动性在0 h、12 h显著降低，24 h有所恢复，1周后基本恢复到正常水平。力竭运动组小鼠前脑皮层和海马突触体内游离Ca2+浓度在0 h、12 h和24 h后显著增加，1周后前脑皮层和海马突触体内游离Ca2+浓度明显回落。力竭游泳运动所致小鼠运动性中枢疲劳的产生和恢复可能与突触体膜流动性和突触体内游离Ca2+浓度的变化密切相关。