研究目的：本实验通过在体多通道同步记录的手段，记录运动疲劳后大鼠自主行为能力、步态协调能力以及运动疲劳不同时间点黑质、纹状体和皮层局部场电位（LFPs）不同状态下的变化，分析运动疲劳对大鼠自主行为能力、步态协调能力以及黑质、纹状体、皮层神经通路的影响，探究运动疲劳后黑质-纹状体多巴胺能（NSDA）通路对皮层信息编码的影响。

研究方法：选用成年雄性Wistar大鼠随机分为行为学组、电生理组和免疫组化组。行为学组随机分为旷场组和错步组，免疫组化组内随机分为安静对照组（CG）、1天运动疲劳组（1FG）、7天运动疲劳组（7FG）和24h恢复组（24RG）。采用实验室改良的Bedford方案建立7天跑台运动疲劳模型，行为学组和电生理组采样时间为运动疲劳前（pre）、1天（post-1D）、7天（post-7D）运动疲劳即刻以及恢复24h（post-24H）。（1）采用旷场测试（OFT）和错步测试评价大鼠自主行为能力、步态协调能力。（2）电生理组将梯度电极分别埋植在背外侧纹状体（STR）、黑质致密部（SNc）和皮层M1区，手术恢复一周后，进行电信号的采集。（3）采用Cerebus在体多通道记录系统记录在进行过程中黑质、纹状体和皮层M1区神经元LFPs。（4）采用免疫组织化学检测背外侧纹状体D1DR在纹状体背外侧区的表达情况。

研究结果：（1）运动疲劳后大鼠自主运动能力显著降低，与pre相比，post-1D和post-7D大鼠的运动距离、平均速度、快速运动时间和最大速度显著减少（P<0.05），大鼠跨越方格次数显著减少（P<0.05），24h后部分恢复；大鼠探索能力随疲劳程度的加深而降低，与pre相比，post-1D和post-7D大鼠后肢站立次数显著减少（P<0.05），并且中心和外周区域有着相同的变化趋势。（2）运动疲劳后大鼠步态协调能力显著下降，与pre相比，post-7D大鼠大鼠通过错步仪时间显著增加（P<0.05）；post-7D大鼠前肢、后肢和尾部错误时间显著增加（P<0.05）；post-7D大鼠前肢、后肢和尾部错误次数显著增加（P<0.05）。（3）在运动疲劳后，SNc、STR和M1各频段的能量值均有所升高，随着疲劳程度的加深能量值也随之增加。与pre相比，post-7D大鼠SNc区α频段功率谱密度（PSD）值均有所升高（P<0.05），post-7D大鼠STR区α、β频段PSD值均有所升高（P<0.05），post-7D大鼠M1区α、β频段PSD值均有所升高（P<0.05），恢复24h后出现一定程度的降低。（4）与无运动期间相比，pre、post-1D、post-7D和post-24H大鼠运动期间黑质、纹状体α、β频段PSD值均显著降低（P＜0.05）；不同时间点大鼠运动期间皮层α频段PSD值均显著降低（P＜0.05），pre、post-1D、post-24H大鼠运动期间β频段PSD值均显著降低（P＜0.05）。（5）运动疲劳后，背外侧纹状体DA受体表达显著降低，与CG相比，1FG和7FG大鼠STR细胞AOD值显著降低（P<0.05）。

研究结论：（1）运动疲劳后，大鼠自主行为能力、探索能力和步态协调能力下降，皮层M1区α、β频段PSD值在运动疲劳后显著升高，24h恢复后部分降低，提示皮层M1区信息编码异常可能导致大鼠产生运动疲劳。（2）黑质、纹状体α、β频段PSD值在运动疲劳后显著升高，24h恢复后部分降低，与无运动期间相比，大鼠运动期间黑质、纹状体和皮层α、β频段PSD值存在显著降低，背外侧纹状体D1DR表达量显著降低，提示运动疲劳后α、β频段PSD值异常增高不是由于大鼠的行为活动引起，NSDA通路信息编码的变化可能是皮层M1信息编码异常的原因之一。

Objective: In this experiment, the multi-channel simultaneous recording in vivo was used to record the exercise capacity and the changes of localized field potentials (LFPs) in SNc, STR, and M1 of rats under different conditions. It revealed the influence of exercise-induced fatigue on locomotor activity, gait coordination and SNc, STR, and M1 neural pathways in rats. It aims to found the effects of nigro-striatal dopaminergic (NSDA) pathway on cortical information coding after exercise-induced fatigue.

Method: Adult male rats were randomly divided into behavior groups, electrophysiological groups, and immunohistochemical groups. Behavioral group was randomly divided into two groups to evaluate the exercise ability of rats by open field test and foot fault test. The immunohistochemical group was randomly divided into control group (CG), 1 day (1FG), 7 day exercise-induced fatigue group (7FG), and a 24h recovery group (24RG). 7 day exercise model was established by electric treadmill. The sampling time of behavior groups and electrophysiological groups was pre-exercise-induced fatigue (pre), 1 day (post-1D), 7 days (post-7D) exercise-induced fatigue immediately and recovery 24h (post-24H). (1) Open field test and foot fault test were used to evaluate the locomotor activity and gait coordination ability in rats. (2) The electrophysiological group implanted gradient electrodes in the STR, SNc, and M1. (3) After one week of surgery, Cerebus in-vivo multichannel recording system was used to record the LFPs of the STR, SNc, and M1. (4) Immunohistochemistry was used to detect the expression of D1DR in the dorsal lateral striatum of the striatum.

Results: (1) It was significantly reduced on locomotor activity after exercise-induced fatigue. Compared with pre, the distance, average speed, fast time, max speed and entries in squares of post-1D and post-7D rats significantly decreased (P<0.05), and partially recovered after 24h. It was significantly decreased on exploratory ability with the deepening of fatigue. Compared with pre, the rearing number of post-1D and post-7D significantly decreased (P<0.05), and central and peripheral areas had the same trend. (2) It was significantly reduced on gait coordination ability after exercise-induced fatigue. Compared with pre, the crossing time was significantly increased in the post-1D and post-7D rats (P<0.05). It was increased significantly in the error time and number of front, rear and tail (P<0.05). (3) After exercise-induced fatigue, the energy value of each band of STR, SNC, and M1 all increased, and the energy value increased with the deepening of fatigue. Compared with pre, the α bands power spectrum density (PSD) values of SNc were increased in post-7D (P<0.05). The α and β bands PSD values of STR and M1 were increased in post-7D (P<0.05), and decreased to a certain extent after 24 hours of recovery. (4) Compared with non- locomotor activity, the α and β bands PSD values of SNc and STR was significantly decreased in the pre, post-1D, post-7D rats and post-24H (P<0.05). The α bands PSD values of M1 was significantly decreased at different time points (P<0.05). The β bands PSD values of M1 was significantly decreased in the pre, post-1D and post-24H (P<0.05). (5) Compared with CG, the AOD value of STR cells in 1FG and post-7D rats was significantly reduced.

Conclusion: (1) We found that the locomotor activity, exploration ability and gait coordination ability were declined after exercise-induced fatigue. The α and β bands PSD values of the M1 was increased. It is suggested that abnormal coding of information in cortical M1 region may cause exercise-induced fatigue in rats. (2) The α and β bands PSD values of SNc and STR were increased. Compared with non- locomotor activity, the α and β bands PSD values of SNc and STR was significantly decreased. The D1DR expression significantly reduced in dorsal lateral striatum. It is suggested that the abnormal increase in α and β band PSD values was not caused by behavioral activities in rats and the change of the coding of the NSDA pathway information may be one of the reasons for the insufficient driving of the cortical M1 information.