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目的:通过观察运动干预对PD模型大鼠纹状体突触超微结构、Glu浓度、D2DR及NMDAR1表达的影响,揭示运动调节PD大鼠皮层-纹状体Glu能神经传递的机制。方法:选用清洁级雄性SD大鼠,随机分为假手术安静组、假手术运动组、帕金森安静组、帕金森运动组,每组18只。采用6-OHDA于内侧前脑束单点注射建立PD大鼠模型,假手术组给予同等剂量生理盐水。术后24 h对运动组大鼠进行运动干预,运动方案为11 m/min,30 min/d,5 d/周,4周。采用透射电子显微镜技术观察皮层-纹状体突触的超微结构,高效液相色谱法(HPLC)检测纹状体Glu浓度,免疫组化与免疫印迹技术观察纹状体D2DR及NMDAR1表达变化。结果:PD运动组大鼠纹状体穿通型突触占不对称突触的比例较PD组明显降低(P<0.05)。PD运动组大鼠纹状体Glu浓度较PD组显著下降(P<0.01)。PD运动组大鼠纹状体D2DR与NMDAR1的表达较PD组显著增加(P<0.05,P<0.05)。结论:运动干预改善了PD模型大鼠皮层-纹状体Glu能神经传递效能,可能与DA对Glu能突触活性的调节作用增强有关。 相似文献
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《European Journal of Sport Science》2013,13(2):87-91
Abstract Possible peripheral mechanisms of fatigue have been widely documented, including the depletion of muscle glycogen and the loss of body fluids. The notion that the brain may be intimately involved in the fatigue process is not a new one, but recently possible neurobiological mechanisms involved in this response have been investigated. Changes in central neurotransmission occur during exercise that may result in feelings of tiredness, lethargy, and a loss of motivation to continue exercise, contributing to the development of fatigue. There is evidence that manipulation of the neurotransmitters serotonin, dopamine, and noradrenaline, through the administration of pharmacological agents, may delay the onset of fatigue during prolonged exercise, particularly when performing in a warm environment. Supplementation with branched-chain amino acids and tyrosine can influence perceived exertion and some measures of mental performance, but the results of several apparently well-controlled laboratory studies have not demonstrated a positive effect on exercise capacity under temperate conditions. The ergogenic effects of carbohydrate and caffeine are well documented, but often little attention is paid to the central effects of these nutrients. Carbohydrate ingestion has been demonstrated to alter brain activity and cerebral metabolism, factors that may be important in the development of fatigue and the maintenance of skill performance. There is strong evidence for a positive effect of caffeine on exercise performance, with recent data highlighting the role of central adenosine as a mediator of this response. 相似文献
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