Memory persistence is a fundamental cognitive process for guiding behaviors and is considered to rely mostly on neuronal and synaptic plasticity. Whether and how astrocytes contribute to memory persistence is largely unknown. Here, by using two-photon Ca²⁺ imaging in head-fixed mice and fiber photometry in freely moving mice, we show that aversive sensory stimulation activates α7-nicotinic acetylcholine receptors (nAChRs) in a subpopulation of astrocytes in the auditory cortex. We demonstrate that fear learning causes the de novo induction of sound-evoked Ca²⁺ transients in these astrocytes. The astrocytic responsiveness persisted over days along with fear memory and disappeared in animals that underwent extinction of learned freezing behavior. Conditional genetic deletion of α7-nAChRs in astrocytes significantly impaired fear memory persistence. We conclude that learning-acquired, α7-nAChR-dependent astrocytic responsiveness is an integral part of the cellular substrate underlying memory persistence.

记忆持久性是指导行为的基本认知过程，被认为主要依赖于神经元和突触可塑性。星形胶质细胞是否以及如何促进记忆持久性在很大程度上是未知的。在这里，通过在头部固定的小鼠中使用双光子 Ca 2+ 成像和在自由移动的小鼠中使用纤维光度测定法，我们表明厌恶的感觉刺激激活了听觉皮层星形胶质细胞亚群中的 α7-烟碱型乙酰胆碱受体 (nAChRs ) ^{。我们证明恐惧学习会导致声音诱发 Ca 2+}的从头诱导这些星形胶质细胞中的瞬变。星形胶质细胞的反应与恐惧记忆一起持续了数天，并在经历了习得的冻结行为灭绝的动物中消失了。星形胶质细胞中 α7-nAChRs 的条件性基因缺失显着损害了恐惧记忆的持久性。我们得出结论，学习获得性、α7-nAChR 依赖性星形胶质细胞反应性是记忆持久性细胞底物不可或缺的一部分。