Xiang Liyang, Zhao Yulu, Li XinRui, Shi Ran, Zhou Wen, Xu Xiaohang, Hu Yifan, Xu Qianyun, Chen Yaodan, Ma Jin, He Xiao, Shen Weida
School of Medicine, Nankai University, Tianjin 300071, China; Key Laboratory of Novel Targets and Drug Study for Neural Repair of Zhejiang Province, School of Medicine, Hangzhou City University, Hangzhou 310015, China; Zhejiang Key Laboratory of Intelligent Rehabilitation and Translational Neuroelectronics, Hangzhou 311121, China.
Key Laboratory of Novel Targets and Drug Study for Neural Repair of Zhejiang Province, School of Medicine, Hangzhou City University, Hangzhou 310015, China.
Neuroscience. 2025 Jan 9;564:306-318. doi: 10.1016/j.neuroscience.2024.11.033. Epub 2024 Nov 17.
Exercise-induced fatigue (EF) is characterized by a decline in maximal voluntary muscle force following prolonged physical activity, influenced by both peripheral and central factors. Central fatigue involves complex interactions within the central nervous system (CNS), where astrocytes play a crucial role. This study explores the impact of astrocytic calcium signals on EF. We used adeno-associated viruses (AAV) to express GCaMP7b in astrocytes of the dorsal striatum in mice, allowing us to monitor calcium dynamics. Our findings reveal that EF significantly increases the frequency of spontaneous astrocytic calcium signals. Utilizing genetic tools to either enhance or reduce astrocytic calcium signaling, we observed corresponding decreases and increases in exercise-induced fatigue time, respectively. Furthermore, modulation of astrocytic calcium signals influenced corticostriatal synaptic plasticity, with increased signals impairing and decreased signals ameliorating long-term depression (LTD). These results highlight the pivotal role of astrocytic calcium signaling in the regulation of exercise-induced fatigue and synaptic plasticity in the striatum.
运动诱导的疲劳（EF）的特征是长时间体力活动后最大自主肌肉力量下降，这受到外周和中枢因素的影响。中枢疲劳涉及中枢神经系统（CNS）内的复杂相互作用，其中星形胶质细胞起着关键作用。本研究探讨星形胶质细胞钙信号对运动诱导疲劳的影响。我们使用腺相关病毒（AAV）在小鼠背侧纹状体的星形胶质细胞中表达GCaMP7b，从而能够监测钙动力学。我们的研究结果表明，运动诱导的疲劳显著增加了星形胶质细胞自发钙信号的频率。利用基因工具增强或减少星形胶质细胞钙信号，我们分别观察到运动诱导的疲劳时间相应减少和增加。此外，星形胶质细胞钙信号的调节影响皮质纹状体突触可塑性，信号增加会损害长时程抑制（LTD），而信号减少则会改善LTD。这些结果突出了星形胶质细胞钙信号在调节运动诱导的疲劳和纹状体突触可塑性中的关键作用。
