运动疲劳通过基底神经节输出核团损伤大鼠工作记忆能力
Exercise-induced chronic fatigue impairs working memory in rats via basal ganglia output nuclei
金硕 1李鸿扬 1吉宸萱 1祁金顺 2孙丽娜3
作者信息
- 1. 北京师范大学体育与运动学院,北京 100875
- 2. 山西医科大学生理学系细胞生理学教育部重点实验室,太原 030001
- 3. 北京师范大学体育与运动学院,北京 100875;北京师范大学认知神经科学与学习国家重点实验室,北京 100875
- 折叠
摘要
目的:探讨基底神经节输出核团[脚内核(EPN)和黑质网状部(SNr)]内小清蛋白(PV)阳性神经元参与运动疲劳损害工作记忆能力的神经调控机制.方法:采用随机数字法将雄性SD大鼠分为对照组(Control)和疲劳组(Fatigue),选用三级递增负荷跑台训练方案,建立慢性力竭运动疲劳模型.利用Y迷宫自主交替实验评估大鼠的工作记忆能力.免疫组织化学染色观察大鼠EPN和SNr内PV和caspase-3的表达.结果:Y迷宫自主交替实验表明,疲劳组大鼠自主交替正确率较对照组大鼠呈显著性降低(P＜0.05).免疫组织化学染色结果显示,疲劳组大鼠EPN和SNr内PV阳性细胞密度和阳性纤维染色程度与对照组相比均大幅降低(P＜0.05,P＜0.01).同时,疲劳组大鼠EPN和SNr内caspase-3阳性细胞密度明显升高(P＜0.05,P＜0.01).结论:运动疲劳导致大鼠工作记忆能力受损,其机制可能与EPN和SNr内PV阳性神经元凋亡有关.
Abstract
Objective:To investigate possible neuromodulatory mechanisms involved in the involvement of parvalbu-min(PV)expression in the basal ganglia output nuclei,entopeduncular nucleus(EPN)and substantia nigra pars etic-ulata(SNr),in exercise-induced chronic fatigue impairs working memory capacity.Methods:Male SD rats were divid-ed into control group and Fatigue group by random number method,and a three-stage incremental load treadmill training program was selected to establish a chronic exhaustion exercise-induced fatigue rat model.The working memory ability of rats was assessed by the Y-maze autonomous alternation experiment.Immunohistochemical staining was used to ob-serve the expression of parvalbumin(PV)positive neurons and cysteine aspartate-specific protease-3(caspase-3)in EPN and SNr of rats.Results:The accuracy of voluntary alternation in the fatigue group was obviously lower than that in control group(P＜0.05).The results of immunohistochemical staining showed that the density of PV positive neu-rons and the degree of positive fiber staining in EPN and SNr in the fatigue group were obviously lower than those in the control group(P＜0.05,P＜0.01).The number of caspase-3 positive cells per unit area of EPN and SNr in the fa-tigue group was obviously higher than that in the control group(P＜0.05,P＜0.01).Conclusion:The mechanism of impairing working memory in rats caused by exercise-induced chronic fatigue may be related to the apoptosis of PV posi-tive neurons in EPN and SNr.
关键词
运动疲劳/工作记忆/基底神经节输出核团/小清蛋白/caspase-3/大鼠Key words
exercise-induced chronic fatigue/working memory/basal ganglia output nuclei/parvalbumin(PV)/caspase-3/rat引用本文复制引用
基金项目
国家自然科学基金(32000835)
北京师范大学认知神经科学与学习国家重点实验室开放基金(CNLZD2104)
出版年
2024
NETL
NSTL
万方数据