Exercise-induced chronic fatigue impairs working memory in rats via basal ganglia output nuclei / 神经解剖学杂志
Chinese Journal of Neuroanatomy
; (6): 9-15, 2024.
Article
en Zh
| WPRIM
| ID: wpr-1019631
Biblioteca responsable:
WPRO
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.
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Índice:
WPRIM
Idioma:
Zh
Revista:
Chinese Journal of Neuroanatomy
Año:
2024
Tipo del documento:
Article