| Summary: | 碩士 === 高雄醫學大學 === 運動醫學系碩士班 === 102 === Recent studies indicate that exercise have beneficial effects on the central nervous system, such as improving learning and memory, reducing the risk of neurodegenerative diseases, and providing protection against insults. Accumulated evidence show that release of brain-derived neurotrophic factor (BDNF) playing a key role in the adaptation of central nervous system to exercise. Early-life exercise can enhance capacity to evoke memories and reduced risk of neurodegenerative diseases in later life. This long-term effects of exercise-induced BDNF can maintain the structure and function of central nervous system, suggesting that exercise may be a useful method to ameliorate the adverse effects caused by insults in early life. In addition, because the brains of infant baby are more vulnerable to environmental toxic agents, early-life exposure to environmental toxic agents may result in increased risk of neural dysfunction in the adults. Furthermore, evidences suggest that vanadium, an important element in alloy manufacturing, is regarded as a candidate of environmental toxin and may cause health problems in humans. Postnatal exposure to sodium metavanadate (NaVO3) can impair the development of cerebellum by reducing the volume of cerebellar white matter in adult animals. Because exercise-induced BDNF release is assumed to protect against neurodegenerative diseases, therefore, an attempt is made in the present study to evaluate the effects of exercise on ameliorating the neonatal NaVO3 exposure-induced neural dysfunction in young adult rats. Sprague Dawley female rats were treated with NaVO3 (3 mg/kg per day, ip.) or vehicle during lactational period. After weaning (postnatal day 22), the male offspring were trained on treadmill running for 5 weeks. At the age of 2 months (late adolescent), animals were subjected to motor coordination test followed by biochemical examination of BDNF and histological examination of the cerebellum. The results showed that deficit of motor coordination, lower BDNF levels in plasma and cerebellum, and increased dendritic spine density were observed in NaVO3-exposed rats. These results indicated that NaVO3 exposure may interfere the pruning of dendritic spines on the cerebellar Purkinje cells by reducing the release of BDNF, leading to dysfunction of cerebellum. After the five-week aerobic exercise training program, the performances of motor coordination were improved in NaVO3-exposed rats. In addition, levels of BDNF and dendritic spine density were restored in the cerebellum of NaVO3-exposed rats after aerobic exercise. Given the findings of this study, it was proposed that aerobic exercise may provide beneficial effects on ameliorating the altered biochemical and neurobehavioral outcomes in lactational NaVO3-exposed young adult rats.
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