Voluntary exercise and tail shock have differential effects on amphetamine-induced dopaminergic toxicity in adult BALB/c mice.
Voluntary exercise and tail shock have differential effects on amphetamine-induced dopaminergic toxicity in adult BALB/c mice.
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自愿运动和尾部电击对成年 BALB/c 小鼠苯丙胺诱导的多巴胺能毒性具有不同的影响。
DOI：
10.1097/00008877-200609000-00013
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发表时间：
2006
影响因子：
1.6
通讯作者：
Wagner,GeorgeC
中科院分区：
文献类型：
--
作者：
Carlson,KirstenM;Wagner,GeorgeC
运动对帕金森病动物模型具有神经保护作用，促进神经恢复。在目前的研究中，运动对安非他明诱导的多巴胺能毒性的影响被评估在单独饲养的小鼠中，有或没有进入跑步轮。老鼠在跑轮笼中每天大约跑20000转（超过10公里/天）。部分小鼠注射安非他明（18.5 mg/ kgx4），对照组注射生理盐水。安非他明导致老鼠体内90%的多巴胺消耗，不管有没有跑步轮。服用安非他明后，跑步轮活动急剧下降，持续至少7天。食物摄取量、饮水量和体重也显著减少。在注射后1、2、3天或2周，运动的机会并不能促进行为或神经化学的恢复。因此，休克应激（一些强迫运动研究的组成部分）被评估，以确定不运动的应激是否对安非他明有神经保护作用。结果表明，休克应激具有神经保护作用，可减轻安非他明引起的多巴胺耗竭。由此得出结论，自愿跑步不能提供行为或神经保护，也不能促进安非他明引起的多巴胺能毒性的恢复；相反，休克应激后糖皮质激素水平升高与多巴胺消耗减少有关。
Exercise exerts neuroprotective effects and facilitates neural recovery in animal models of Parkinson's disease. In the present studies, effects of exercise on amphetamine-induced dopaminergic toxicity were assessed in mice housed individually either with or without access to run wheels. Mice in run wheel cages ran approximately 20 000 revolutions/day (over 10 km/day). Some mice received amphetamine (18.5 mg/kg× 4 injections) whereas controls received saline. Amphetamine caused a 90% dopamine depletion in mice housed either with or without run wheels. A precipitous drop was seen in run wheel activity following amphetamine, lasting at least 7 days. A significant decrease in food intake, water intake and body weight also occurred. The opportunity to exercise did not facilitate behavioral or neurochemical recovery at 1, 2 or 3 days, or 2 weeks after injections. Therefore, shock stress, a component of some forced exercise studies, was evaluated to determine whether stress without exercise provided neuroprotection against amphetamine. Results indicate that shock stress exerted neuroprotective effects, reducing the amphetamine-induced dopamine depletion. It is concluded that voluntary running does not afford either behavioral or neuroprotection nor facilitate recovery from amphetamine-induced dopaminergic toxicity; rather, elevated glucocorticoid levels following shock stress were associated with a reduction in the dopamine depletion.