摘要
跑台运动可以改善脑卒中大鼠的学习记忆能力,然而机制尚不清楚。因此,通过观察4周强迫跑台运动对短暂大脑中动脉(MCAO,middle cerebral artery occlusion)栓塞大鼠空间学习记忆能力、血浆皮质酮(Cort)及纹状体氨基酸水平和脑源性神经营养因子BDNF(brain-derived neurotrophic factor)表达的影响,研究跑台运动改善MCAO大鼠学习记忆功能的可能机制。方法:45只SD大鼠随机分为假手术组、脑缺血模型组及脑缺血运动组,脑缺血模型组及运动组大鼠制备MCAO短暂缺血模型,随后脑缺血运动组大鼠进行4周跑台运动。跑台运动结束后通过水迷宫实验测试所有大鼠学习记忆能力的变化,随后放射免疫法测试大鼠血浆Cort含量,采用高效液相-电化学方法检测纹状体Glu、GABA的含量,用免疫组织化学结合图像半定量方法对纹状体BDNF神经元的数量及面积进行测量和分析。结论:大脑中动脉(MCAO)短暂缺血大鼠的学习记忆能力可以通过进行长期跑台运动得到改善,其原理极有可能与长期跑台运动上调纹状体BDNF的表达,拮抗HPA轴功能亢进及兴奋性氨基酸的毒性,抑制神经元的坏死及凋亡,促进脑缺血后损伤神经元的修复有关。
Treadmill exercise may enhance the recovery of impaired memory function in stroke rats.However,the mechanisms underlying these beneficial effects are not yet known.Therefore,the purpose of this study was to investigate the effects of the 4-week forced treadmill exercise on the learning and memory,the blood plasma cort content,amino acid levels and BDNF expression within striatum of brain after MCAO(transient middle cerebral artery occlusion)rats,inquiring into the possible mechanism of treadmill exercise improving learning and memory of MCAO rats.Methods:45male SD rats were randomly allocated to 3groups,sham operation group(SO),cerebral ischemia model group(CM)and cerebral ischemia exercise group(CE).The rats of CM and CE group rats were submitted to the transient middle cerebral artery occlusion,and then the CE group rats received 4-week forced treadmill exercise.Then all rats were submitted to behavioral testing for spatial memory by the Morris water maze;then the blood plasma cort content was detected by radioimmunoassay.Subsequently the concentration of Glu and GABA were examined by high performance liquid-electrochemical detection and BDNF expression within striatum was detected and analysised by using immuneohistochemical method.Conclusion:Treadmill exercise may improve the learning and memory ability after MCAO rats,its mechanism might be that treadmill exercise upregulate BDNF expression,overactive HPA axis antagonism and decrease Glu neurotoxicity within striatum,inhibit neuronal necrosis and apoptosis and promote the repair of damage neurons.
出处
《首都体育学院学报》
CSSCI
北大核心
2016年第6期572-576,共5页
Journal of Capital University of Physical Education and Sports
基金
中北大学科学基金(2015-2016)