• Zhonghua yi xue za zhi · Mar 2012

    [Effects of exercise training on synaptic plasticity in rats with focal cerebral infarction].

    • Hai-qing Zheng, Xi-quan Hu, Jie Fang, San-qiang Pan, Li-li Li, and Li-ying Zhang.
    • Department of Rehabilitation Medicine, Third Affiliated Hospital, Sun Yat-sen University, Guangzhou 510630, China.
    • Zhonghua Yi Xue Za Zhi. 2012 Mar 6; 92 (9): 628-33.

    ObjectiveTo examine the roles of exercise training in the improvement of damaged neural function and synaptic plasticity.MethodsAn infarction model was induced by left middle cerebral artery occlusion (MCAO). A total of 70 adult Sprague-Dawley rats were randomly divided into 3 groups: physical exercise group (n = 30) undergoing running wheel exercise daily after MCAO, control group (n = 30) and sham-operated group (n = 10). The latter two groups were fed in standard cages without any special training exercise. The rats were scarified at Days 3, 7, 14, 21 and 35 for the evaluation of neural function by neurological severity scores (NSS). And the synaptic ultrastructures at peri-infarction region were examined by specific marker synaptophysin (SYN).ResultsSynaptic ultrastructures at peri-infarction region were observed in both the control and exercise training groups. The presynaptic and postsynaptic membranes were relatively intact. And the presynaptic membranes had more synaptic vesicles from Day 7 post-ischemia. The number of SYN positive cells significantly increased in the exercise training group (21 d: 0.8 ± 0.1; 35 d: 0.7 ± 0.1) versus those in the control group (21 d: 0.4 ± 0.1; 35 d: 0.5 ± 0.1) at Days 21 and 35 post-ischemia (P < 0.05). Moreover, the neurological severity scores in the exercise training group (7 d: 7.8 ± 0.8; 14 d: 5.6 ± 0.8; 21 d: 3.3 ± 0.8; 35 d: 3.0 ± 0.8) showed a quicker declination versus those in the control group (7 d: 8.8 ± 0.7; 14 d: 7.7 ± 0.9; 21 d: 6.9 ± 0.8; 35 d: 4.2 ± 0.8) from Day 7 post-ischemia (P < 0.05).ConclusionExercise training plays an important role in the recovery of damaged neural function and synaptic plasticity after cerebral infarction in rats.

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