Exercise-induced Fatigue Influenced Striatal Neuron’s Synaptic Ultrastructure and D2DR Intervention Role in Rat

Objective:Through investigating dorsolateral striatum (DLS) synaptic ultrastructural change and D2DR antagonist/agonist effect on autonomic activity in exercise-induced fatigue rats, explore the central regulation role of substantia nigra striatum pathway. Methodology:Male Wistar rats were randomly divided into control group (CG) , 1-day fatigue group (1FG) , 3-day fatigue group (3FG) , 7-day fatigue group (7FG) , 24-hour recovery group (24RG) and 48-hour recovery group (48RG) . The synaptic ultrastructure was observed by transmission electron microscopy, the expression of PSD-95 protein was detected by immunohistochemistry and the correlation between ultrastructure and PSD-95 was analyzed. D2DR antagonist and agonist were used to interfere the autonomic exercise of rats with Open Field Test. Results: (1) The width of synaptic clefts of DLS decreased significantly in 1FG compared with CG (P< 0.01) , and the density of 3FG and 7FG decreased significantly (P<0.05) compared with CG and 1FG; (2) Compared with CG and 1FG, expression of PSD-95 protein in 24 RG was significantly increased (P<0.05) ; (3) The total exercise distance of each group decreased gradually with the increase of exercise intensity, and the rest returned to a quiet level. Rats exhaustion time was significantly shortened after injection of D2DR antagonist (P< 0.01) , while the agonist intervention significantly increased the exhaustion time (P< 0.01) . Conclusions:PSD-95 has no correlation with the degree of exercise-induced fatigue, while exercise-induced fatigue reduced the ability of rats' autonomic activity. D2DR antagonist intervention made the exercise-induced fatigue condition deeply while D2DR agonist has convers role. The regulation of D2DR may be related to synaptic plasticity of dopaminergic microcirculation in the substantia nigra striatum, it suggests that D2DR can be selected as an important target for regulation exercise-induced fatigue.