Inoue Koshiro, Okamoto Masahiro, Fukuie Takemune, Soya Hideaki, Yamaguchi Akihiko
School of Rehabilitation Sciences, Health Sciences University of Hokkaido, Ishikari-Tobetsu, Hokkaido, Japan.
Laboratory of Exercise Biochemistry and Neuroendocrinology, Institute of Health and Sport Sciences, University of Tsukuba, Ibaraki, Japan.
PLoS One. 2025 Jul 18;20(7):e0328128. doi: 10.1371/journal.pone.0328128. eCollection 2025.
Acute moderate-intensity exercise (AME) after learning has been reported to exogenously boost consolidation of hippocampus-dependent memory, resulting in improved long-term persistence. However, the neuronal mechanism remains poorly understood. Short-term, hippocampus-dependent memory produced by weak encoding can be transformed into long-term memory through an immediate, strong behavioral event, which causes overlapping activation of the hippocampus. Hippocampal de novo protein synthesis is essential for achieving memory consolidation in this way. As AME activates the hippocampus, enhanced memory consolidation through post-learning AME may also be mediated by protein synthesis in the hippocampus. To test this hypothesis, this study first attempted to establish a rat model for enhancing memory consolidation via post-learning AME with the object location (OL) test, a hippocampus-dependent spatial memory task. This study used adult male Sprague-Dawley rats, and the AME load was based on the running speed corresponding to the rats' lactate threshold (20 m/min) for 20 min. We then examined the effects of the protein synthesis inhibitor anisomycin (ANI), injected into the dorsal hippocampus, on AME-induced OL memory consolidation. In the OL test, the OL memory encoded with 5 min of learning was retained for at least 1 hr but was lost after 24 hr. With a single bout of AME immediately after the 5 min of OL learning, the memory persisted for 24 hr, indicating AME-induced memory consolidation. The AME-induced OL memory consolidation did not occur when ANI was injected into the dorsal hippocampus immediately or 4 hr after OL learning. These findings support the hypothesis that post-learning AME-induced memory consolidation depends on new-protein synthesis in the dorsal hippocampus and highlight the value of AME after learning as a strategy for enhancing memory consolidation. This is a potential base model for future research examining the mechanism behind boosting memory consolidation with exercise.
据报道，学习后进行急性中等强度运动（AME）可外源性增强海马体依赖性记忆的巩固，从而改善长期记忆持久性。然而，其神经元机制仍知之甚少。由弱编码产生的短期海马体依赖性记忆可通过即时的强烈行为事件转化为长期记忆，该事件会导致海马体的重叠激活。海马体从头合成蛋白质对于以这种方式实现记忆巩固至关重要。由于AME会激活海马体，学习后AME增强的记忆巩固也可能由海马体中的蛋白质合成介导。为了验证这一假设，本研究首先尝试通过物体位置（OL）测试（一种海马体依赖性空间记忆任务）建立一个通过学习后AME增强记忆巩固的大鼠模型。本研究使用成年雄性Sprague-Dawley大鼠，AME负荷基于对应大鼠乳酸阈值（20米/分钟）的跑步速度，持续20分钟。然后，我们研究了注射到背侧海马体的蛋白质合成抑制剂茴香霉素（ANI）对AME诱导的OL记忆巩固的影响。在OL测试中，通过5分钟学习编码的OL记忆至少保留1小时，但在24小时后消失。在OL学习5分钟后立即进行单次AME，记忆持续24小时，表明AME诱导了记忆巩固。当在OL学习后立即或4小时后将ANI注射到背侧海马体时，AME诱导的OL记忆巩固未发生。这些发现支持了以下假设，即学习后AME诱导的记忆巩固依赖于背侧海马体中的新蛋白质合成，并突出了学习后AME作为增强记忆巩固策略的价值。这是未来研究运动增强记忆巩固背后机制的潜在基础模型。
