中文摘要：

目的：通过观察运动大鼠力竭前后“黑质/苍白球-丘脑-皮质”通路各核团5-羟色胺1B受体（5-HT1B）及多巴胺1型受体（D1DR）的蛋白表达水平，探讨“黑质/苍白球-丘脑-皮质”通路调控运动疲劳发生、发展的中枢机制。方法：24只雄性Wistar大鼠，随机分为安静对照组、力竭即刻组、恢复90min组，每组8只。采用免疫组织化学技术对不同组别5-HT1B和D1DR的蛋白表达水平进行检测。结果：与安静组对照组相比，力竭即刻组、恢复90min组大鼠黑质网状部及苍白球内侧部5-HT1B受体阳性细胞R值及平均光密度（AOD）值均显著减少（P＜0.05），D1DR受体阳性细胞R值及AOD值均显著增加（P＜0.05）；力竭即刻组、恢复90min组大鼠丘脑腹外侧核5-HT1B受体阳性细胞R值及AOD值均显著增加（P＜0.05，P＜0.01）；在大鼠皮质辅助运动区，力竭即刻组、恢复90min组5-HT1B受体阳性细胞R值及AOD值均显著增加（P＜0.05），D1DR受体阳性细胞R值及AOD值均显著减少（P＜0.05）。结论：力竭运动过程中“黑质网状部/苍白球内侧部-丘脑-皮质”各核团5-HT1B及D1DR受体蛋白表达变化引起神经递质释放量改变，进而影响神经元电活动兴奋性，可能是“黑质网状部/苍白球内侧部-丘脑-皮质”通路调节运动疲劳及运动能力的重要途径之一。

英文摘要：

Objective： To observe the changes of 5-HT1B and D1DR expression in nucleus of “SNr/GPi-VL-SMA” pathway in pre and post-exhaustive exercise, and investigate the central mechanism of “SNr/GPi-VL-SMA” pathway modulating the occurrence and development of exercise-induced fatigue. Method： Twenty-four male Wistar rats were randomly divided into control group （CG）, immediately after exhaustion group （EG）, and 90min after recovery group （RG）, each consists of 8 rats. The expression level of 5-HT1B and D1DR receptors in each group were observed with the immunohistochemistry technique. Result： Compared with CG, the positive cell area/scanning area value （R value） and the average optical density value （AOD value） of 5-HT1B receptor in SNr and GPi of the EG and RG rats both decreased significantly （P〈0.05）, while the R value and AOD value of D1DR both increased significantly（P〈0.05）. The R value and AOD value of 5-HT1B receptor in VL of EG and RG rats increased significantly（P〈0.05, P〈0.01）. In SMA, the R value and AOD value of 5-HT1B receptor of EG and RG rats increased significantly （P〈0.05）, while, the R value and AOD value of D1DR receptor decreased significantly （P〈0.05）. Conclusion： Changes of 5-HT1B receptor and D1DR receptor expression in the nuclei of ‘SNr/GPi-VL-SMA’ pathway caused the changes of the neurotransmitters release, thus affecting the excitability of the electrical activity of neurons, this might be one of the important ways for ‘SNr/GPi-VL-SMA’ pathway modulating the exercise-induced fatigue and exercise performance.