深圳湾实验室甘文标团队取得一项新突破。他们提出了星形胶质细胞Ca²⁺通过限制运动学习期间树突的重复活动来防止突触失联。2025年10月13日出版的《自然—神经科学》发表了这项成果。

该课题组发现运动训练诱导第5层锥体神经元顶端树突突触增强，以及单母细胞运动皮层星形细胞Ca²⁺升高。减少星形胶质细胞Ca²⁺导致运动训练期间突触失联和随后的性能改善损伤。值得注意的是，突触失联发生在部分具有重复树突Ca²⁺活性的树突上。在这些树突上，在树突Ca²⁺活性之前活跃的树突棘经历了CaMKII依赖性的大小减少。此外，腺苷受体的激活阻止了重复的树突Ca²⁺活性和由星形细胞Ca²⁺减少引起的突触失联，这表明星形细胞释放的ATP和腺苷信号参与了这一过程。总之，这些发现揭示了星形细胞Ca²⁺通过限制学习过程中重复的树突活动来防止突触失联的功能。

研究人员表示，星形胶质细胞Ca²⁺活性调节活动依赖性突触可塑性，但其在活脑学习相关突触变化中的作用尚不清楚。

附：英文原文

Title: Astrocytic Ca2+ prevents synaptic depotentiation by limiting repetitive activity in dendrites during motor learning

Author: Lai, Baoling, Yuan, Deliang, Xu, Zhiwei, Zhang, Feilong, Li, Ming, Martn-vila, Alejandro, Chen, Xufeng, Chen, Kai, Ouyang, Kunfu, Yang, Guang, Chao, Moses V, Gan, Wen-Biao

Issue&Volume: 2025-10-13

Abstract: Astrocytic Ca2+ activity regulates activity-dependent synaptic plasticity, but its role in learning-related synaptic changes in the living brain remains unclear. We found that motor training induced synaptic potentiation on apical dendrites of layer 5 pyramidal neurons, as well as astrocytic Ca2+ rises in the mouse motor cortex. Reducing astrocytic Ca2+ led to synaptic depotentiation during motor training and subsequent impairment in performance improvement. Notably, synaptic depotentiation occurred on a fraction of dendrites with repetitive dendritic Ca2+ activity. On those dendrites, dendritic spines that were active before dendritic Ca2+ activity underwent CaMKII-dependent size reduction. In addition, the activation of adenosine receptors prevented repetitive dendritic Ca2+ activity and synaptic depotentiation caused by the reduction of astrocytic Ca2+, suggesting the involvement of ATP released from astrocytes and adenosine signaling in the processes. Together, these findings reveal the function of astrocytic Ca2+ in preventing synaptic depotentiation by limiting repetitive dendritic activity during learning.

DOI: 10.1038/s41593-025-02072-4

Source: https://www.nature.com/articles/s41593-025-02072-4