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中文题名:

 运动疲劳及D2DR干预对大鼠皮层-纹状体及黑质电活动的影响    

姓名:

 王晓昕    

保密级别:

 公开    

论文语种:

 中文    

学科代码:

 040302    

学科专业:

 运动人体科学    

学生类型:

 硕士    

学位:

 教育学硕士    

学位类型:

 学术学位    

学位年度:

 2018    

校区:

 北京校区培养    

学院:

 体育与运动学院    

研究方向:

 运动生理学    

第一导师姓名:

 侯莉娟    

第一导师单位:

 北京师范大学体育与运动学院    

提交日期:

 2018-06-25    

答辩日期:

 2018-05-23    

外文题名:

 THE EFFECT OF EXERCISE-INDUCED FATIGUE AND D2DR INTERVENTION ON THE ELECTRICAL ACTIVITY OF CORTICOSTRIATAL AND SUBSTANTIA NIGRA IN RATS    

中文关键词:

 运动疲劳 ; β振荡 ; 相位同步 ; D2DR ; VMAT2    

中文摘要:
研究目的:通过观察运动疲劳后大鼠皮层M1-纹状体通路的局部场电位(Local field potential, LFPs)及黑质致密部DA能神经元电活动的变化情况,以及DA 信号系统在运动疲劳后代谢表达变化,分析皮层M1-纹状体同步振荡的相干性及黑质DA能神经元各频段放电变化,探讨皮层-纹状体通路电信号编码在运动疲劳中枢调控中的机制及其与黑质-纹状体DA系统的协同作用。 研究方法:采用Wistar大鼠建立运动疲劳模型,随机分为电生理组(N=12)、D2DR激动剂干预组(N=6)及蛋白表达组(N=9),组内又根据不同的运动阶段分为对照组(CG)、7天力竭运动即刻组(7FG)以及7天重复力竭运动24h恢复组(24RG)。采用在体多通道实时同步记录技术,结合实时视频录像记录M1-纹状体及黑质LFPs,分析皮层M1-纹状体同步振荡的相干性、D2DR激动剂作用后各频段放电情况及黑质不同频段在运动疲劳前后放电变化;采用免疫组化检测纹状体背外侧区DA受体及相关转运体蛋白在运动疲劳前后的表达情况。 研究结果: 1)与CG组比较,7FG组皮层M1区及纹状体α及β振荡增强(P<0.05);恢复24小时后较7FG组PSD值显著下降(P<0.05);且皮层M1-纹状体α及β振荡相干系数变大(P<0.05),同步性增强;与7FG组比较,24RG组相干系数及STWA比率均显著下降(P<0.05);2)与CG组比较,7FG组黑质致密部θ频段(4-7Hz)、α频段(7-13Hz)及β频段(15-30Hz)PSD值升高,与7FG比较,24RG组的PSD值降低,且差异均具有显著性(P < 0.05);3)和CG组比较可知,7FG组纹状体背外侧区D2DR蛋白表达降低,VMAT2蛋白表达上调,差异具有显著性(P<0.05);与7FG组比较可得,24RG组背外侧纹状体区D1DR表达显著降低(P<0.05)。 研究结论:运动疲劳后,黑质电活动增强,而D2DR蛋白表达下降,造成纹状体GABA能神经元活动增强,反馈至皮层,致使皮层的信息整合加工输出发生改变,进而影响大鼠行为活动能力。皮层M1和纹状体脑区之间同步振荡活动的改变可能是运动疲劳症状产生的原因之一,且D2DR作为DA信号系统的关键受体,可视为延缓运动疲劳现象产生的药物干预靶点。
外文摘要:
Purpose: In this experiment, the phase synchronization oscillation activity of Local field potential (LFPs) was observed in the corticostriatal pathway and electrical activity change in substantia nigra compact after exercise-induced fatigue of rats. In combination with the changes of DA signal system, the role of corticostriatal pathway electrical signal coding in the central regulation of exercise-induced fatigue and the effect of nigrostriatal DA system on it were investigated. Methods: Wistar rats were used to establish the model of exercise-induced fatigue. The rats were divided into control group (CG), 7 days fatigue group (7FG) and 24 hour recovery group (24RG). We used in vivo multichannel recording technology to record electrical activity in the M1, striatum and substantia nigra compact of rats and observed the electrophysiological changes. The coherence of M1 and striatal synchronization oscillations and the effect of D2DR agonist intervention was also analyzed. We also detected the expression of DA receptor and related transporter proteins in the dorsolateral striatum before and after exercise-induced fatigue by immunohistochemistry. Results: 1)Electrophysiological parameters of M1 and striatum show that power spectral density of α and β band was higher in 7FG than CG rats (P<0.05); After 24 hours of recovery, the PSD value decreased significantly compared with the 7FG group (P<0.05); And the coherence value and phase index of β oscillation between motor cortical and striatal was both increased in 7FG rat (P<0.05); The coefficient of coherence and the STWA ratio in the 24RG were significantly decreased than 7FG group (P<0.05); 2) Compared with the CG group, the power spectral density of the θ, α and β band of the SNc was increased after seven days of exhaustion exercise(P < 0.05); After 24 hours of recovery, the PSD value decreased significantly compared with the 7FG group(P<0.05); 3)Compared with CG rats, the expression of D2DR protein in 7FG group was significantly decreased (P<0.05) while the VMAT2 was significantly increased (P<0.05) in the dorsolateral striatum; And the D1DR of the 24RG group was significantly lower than that in the 7FG group (P<0.05). Conclusion: After exercise-induced fatigue, the reduction of D2DR may be one of the reasons for the changes in the thickness of the postsynaptic density. The activity of GABA in the striatum is enhanced, and feedback to the cortex, resulting in the change of the comprehensive information of the cortex, thus affecting the behavior ability of the rat. It is suggested that alterations in electrical signals may be one of the causes of exercise-induced fatigue symptoms. D2DR, as the key receptor of DA signal system, may be a target for exercise-induced fatigue.
参考文献总数:

 110    

开放日期:

 2019-07-09    

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