• Neuroscience · Jan 2025

    Astrocytic calcium signals modulate exercise-induced fatigue in mice.

    • Liyang Xiang, Yulu Zhao, XinRui Li, Ran Shi, Wen Zhou, Xiaohang Xu, Yifan Hu, Qianyun Xu, Yaodan Chen, Jin Ma, Xiao He, and Weida Shen.
    • 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. Electronic address: xiangly@nurotron.com.
    • Neuroscience. 2025 Jan 9; 564: 306318306-318.

    AbstractExercise-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.Copyright © 2024 International Brain Research Organization (IBRO). Published by Elsevier Inc. All rights reserved.

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