中文摘要：

目的：观察运动对帕金森病（PD）模型大鼠纹状体（STR）神经元自发放电活动的影响，揭示运动防治PD的神经电生理机制。方法：清洁级sD大鼠44只分为4组：假手术组（Contr01）、假手术运动组（Con-trol＋Ex）、PD组（PD）和PD运动组（PD＋Ex）。在大鼠内侧前脑束注射6-羟基多巴（6-OHDA）建立右侧PD大鼠模型。运动组术后24 h开始进行跑台训练，11 m／min，30 min／day，5 d／周，共4周。大鼠在造模后第1周、第2周和第4周颈部皮下注射阿朴吗啡（APO）进行旋转行为学测试，记录30 min的旋转次数。采用玻璃微电极胞外记录技术，在体观察各组大鼠STR神经元自发放电活动的变化。结果：APO诱导的旋转行为能力检测，4周后PD组净旋转次数为（282．8 ±32）r／30 min，PD＋Ex组为（226．7±16．2）r／30min，PD＋Ex组较PD组显著减少（P〈0．01）。PD组大鼠神经元自发放电频率较Control组显著升高（P〈0．01），爆发式放电神经元比例显著增多（P〈0．01）。PD＋Ex组大鼠较PD组放电频率显著降低（P〈0．05），爆发式放电神经元比例显著减少（P〈0．05）。结论：早期运动干预能降低PD模型大鼠STR神经元高频放电和爆发式放电神经元比例，抑制STR神经元的过度兴奋，改善PD模型大鼠行为能力。推测：运动引起PD模型大鼠STR神经元兴奋性改变的机制可能与运动神经保护作用降低了6-OHDA对多巴胺（DA）能神经元的毒性损伤以及运动神经可塑性机制调节了皮层一纹状体Glu通路的突触传递有关。

英文摘要：

Objective ： This study observed the effects of exercise on striatum ＇ s neuronal activity in rats with parkin son＇s disease, and aimed to detect the mechanism of preventing and curing parkinson＇ s disease by exercise. Methods： Fortyfour adult male SD rats were randomly divided into four groups： shamoperation group （Control）, shamoperation with exercise group （Control ＋ Ex）, parkinson＇ s disease group （PD） and parkin son＇ s disease group with exercise（ PD ＋ Ex）. 6 OHDA was injected into the right medial forebrain bundle of rats to establish model of parkinson＇ s disease. Rats in exercise group were participated in treadmill exercise 24h after 6 OHDA injection （ 11 m/min, 30 min/day, 5 days/week, and 4 weeks in total）. Behavior evaluation was measured by rotational test induced by apomorphine at the first, second, and fourth week. Striatum＇ s neuronal ac tivity in vivo was observed by extracellular glass microelectrode technique. Results： The number of rotations in duced by apomorphine in PD group （282. 8 ± 32 r/30 min） was higher than that in PD ＋ Ex group （226. 7 ± 16. 2 r/30 min） after 4 weeks （ P 〈 0. 01 ）. Spontaneous frequency and bursting rate of striatum＇ s neuronal activity in PD group were higher than those in control group （ P 〈 0.01 ）, also they were higher than those in PD ＋ Ex group （ P 〈 0. 05 ）. Conclusion： Exercise can decrease the frequency and bursting rate of stratum＇ s neuronal activ ity in rats with parkinson＇ s disease, control hyperexcitability of striatum＇ s neuronal activity, and improve behav iors of rats with parkinson＇ s disease. The authors speculate that the mechanism of changing striatum＇ s neuronalactivity by exercise may be related to the decreased damage of dopaminergic neurons induced by 6 OHDA after exercise, and motor nerve plasticity regulates modulate synaptic transmission in cortexstriatum Glu pathway.