Oligodendrocytes, which form the myelin sheaths that insulate axons, regulate conduction velocity. Myelinated axons make up the brain’s white matter and contribute to the efficiency of information processing by regulating the timing of neural activity. Traditionally, it has been thought that myelin is a static, inactive insulator around the axon. However, recent studies in humans using magnetic resonance imaging have shown that structural changes in the white matter occur during learning and training, suggesting that 1) white matter change depends on neural activity and 2) activity-dependent changes in white matter are essential for learning and behavior. Furthermore, suppression of oligodendrocytes and their progenitor cells leads to deficits in motor learning and remote fear memory consolidation, suggesting a causal relationship between glial function and the learning process. However, for technical reasons, it remains unclear how myelin-generating glia modulate neural circuitry and what underlying mechanisms they employ to affect learning and behavior. Recent advances in optical and genetic techniques have helped elucidate this mechanism. In this review, we highlight evidence that neural activities regulated by myelin plasticity play a pivotal role in learning and behavior and provide further insight into possible therapeutic targets for treating diseases accompanied by myelin impairment.

少突胶质细胞形成隔离轴突的髓鞘，调节传导速度。有髓轴突构成大脑的白质，并通过调节神经活动的时间来提高信息处理的效率。传统上，人们认为髓磷脂是围绕轴突的静态、非活动绝缘体。然而，最近使用磁共振成像对人类进行的研究表明，白质的结构变化发生在学习和训练期间，这表明 1) 白质变化取决于神经活动，2) 白质的活动依赖性变化对学习至关重要和行为。此外，对少突胶质细胞及其祖细胞的抑制导致运动学习和远程恐惧记忆巩固的缺陷，表明神经胶质功能与学习过程之间存在因果关系。然而，由于技术原因，尚不清楚产生髓鞘的神经胶质如何调节神经回路以及它们采用什么潜在机制来影响学习和行为。光学和遗传技术的最新进展有助于阐明这种机制。在这篇综述中，我们强调了由髓鞘可塑性调节的神经活动在学习和行为中发挥关键作用的证据，并为治疗伴有髓鞘损伤的疾病提供了可能的治疗靶点的进一步见解。光学和遗传技术的最新进展有助于阐明这种机制。在这篇综述中，我们强调了由髓鞘可塑性调节的神经活动在学习和行为中发挥关键作用的证据，并为治疗伴有髓鞘损伤的疾病提供了可能的治疗靶点的进一步见解。光学和遗传技术的最新进展有助于阐明这种机制。在这篇综述中，我们强调了由髓鞘可塑性调节的神经活动在学习和行为中发挥关键作用的证据，并为治疗伴有髓鞘损伤的疾病提供了可能的治疗靶点的进一步见解。