PDF(Pubmed)
Abstract：
The striatum plays a crucial role in providing input to the basal ganglia circuit and is implicated in the pathological process of Parkinson\'s disease (PD). Disruption of the dynamic equilibrium in the basal ganglia loop can be attributed to the abnormal functioning of the medium spiny neurons (MSNs) within the striatum, potentially acting as a trigger for PD. Exercise has been shown to mitigate striatal neuronal dysfunction through neuroprotective and neurorestorative effects and to improve behavioral deficits in PD model mice. In addition, this effect is offset by the activation of MSNs expressing dopamine D2 receptors (D2-MSNs). In the current study, we investigated the underlying neurobiological mechanisms of this effect. Our findings indicated that exercise reduces the power spectral density of the beta-band in the striatum and decreases the overall firing frequency of MSNs, particularly in the case of striatal D2-MSNs. These observations were consistent with the results of molecular biology experiments, which revealed that aerobic training specifically enhanced the expression of striatal dopamine D2 receptors (D2R). Taken together, our results suggest that aerobic training aimed at upregulating striatal D2R expression to inhibit the functional activity of D2-MSNs represents a potential therapeutic strategy for the amelioration of motor dysfunction in PD.
摘要：
纹状体在向基底神经节回路提供输入中起着至关重要的作用，并且与帕金森氏病（PD）的病理过程有关。基底神经节环中动态平衡的破坏可归因于纹状体中的多刺神经元（MSN）的异常功能，可能是PD的触发因素。运动已被证明可以通过神经保护和神经修复作用减轻纹状体神经元功能障碍，并改善PD模型小鼠的行为缺陷。此外,这种效应被表达多巴胺D2受体(D2-MSNs)的MSNs的激活所抵消.在目前的研究中,我们研究了这种效应的潜在神经生物学机制.我们的发现表明，运动降低了纹状体中β波段的功率谱密度，并降低了MSN的整体发射频率，特别是在纹状体D2-MSNs的情况下。这些观察结果与分子生物学实验的结果一致，这表明有氧训练特异性增强纹状体多巴胺D2受体（D2R）的表达。一起来看,我们的结果表明,旨在上调纹状体D2R表达以抑制D2-MSNs功能活性的有氧训练是改善PD运动功能障碍的潜在治疗策略.
