Exercise-induced chronic fatigue impairs working memory in rats via basal ganglia output nuclei
10.16557/j.cnki.1000-7547.2024.01.002
- VernacularTitle: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
- Author:
Shuo JIN
1
;
Hongyang LI
;
Chenxuan JI
;
Jinshun QI
;
Lina SUN
Author Information
1. 北京师范大学体育与运动学院,北京 100875
- Keywords:
exercise-induced chronic fatigue;
working memory;
basal ganglia output nuclei;
parvalbumin(PV);
caspase-3;
rat
- From:
Chinese Journal of Neuroanatomy
2024;40(1):9-15
- CountryChina
- Language:Chinese
-
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.
