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

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。

Objective:To investigate possible neuromodulatory mechanisms involved in the involvement of parvalbumin(PV)expression in the basal ganglia output nuclei,entopeduncular nucleus(EPN)and substantia nigra pars eticulata(SNr),in exercise-induced chronic fatigue impairs working memory capacity.Methods:Male SD rats were divided 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 observe 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 neurons 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 fatigue 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 positive neurons in EPN and SNr.