经验塑造大脑结构和功能。神经系统有髓鞘基础设施的活动依赖性调节已成为儿童发育和成年期间适应性变化的一个维度。髓鞘形成是一个丰富的动态过程，神经元活动调节少突胶质细胞前体细胞增殖、少突胶质细胞发生以及某些轴突亚型和神经系统某些区域的髓磷脂结构变化。这种髓磷脂的可塑性以及随之而来的传导速度和电路动力学的变化可以强烈影响神经功能，包括学习和记忆。相反，调节适应性髓鞘形成的机制的破坏可能导致认知障碍。神经元活动对正常少突胶质细胞前体细胞（多种形式的神经胶质瘤的假定细胞起源）的强烈影响表明，髓磷脂可塑性的失调或“劫持”机制同样可以促进这一毁灭性脑癌的生长。事实上，在临床前模型中，神经元活动通过活动调节的旁分泌因子和直接的神经元与神经胶质瘤突触促进多种形式的神经胶质瘤的发病机制。神经胶质瘤与神经回路的突触整合对于肿瘤生长和侵袭至关重要。因此，神经元-少突胶质细胞的相互作用不仅可以调节健康大脑中的神经回路结构和功能，而且神经元-神经胶质瘤的相互作用也在神经胶质恶性肿瘤的发病机制中发挥重要作用。© 2023。Springer Nature Limited。

Experience sculpts brain structure and function. Activity-dependent modulation of the myelinated infrastructure of the nervous system has emerged as a dimension of adaptive change during childhood development and in adulthood. Myelination is a richly dynamic process, with neuronal activity regulating oligodendrocyte precursor cell proliferation, oligodendrogenesis and myelin structural changes in some axonal subtypes and in some regions of the nervous system. This myelin plasticity and consequent changes to conduction velocity and circuit dynamics can powerfully influence neurological functions, including learning and memory. Conversely, disruption of the mechanisms mediating adaptive myelination can contribute to cognitive impairment. The robust effects of neuronal activity on normal oligodendroglial precursor cells, a putative cellular origin for many forms of glioma, indicates that dysregulated or 'hijacked' mechanisms of myelin plasticity could similarly promote growth in this devastating group of brain cancers. Indeed, neuronal activity promotes the pathogenesis of many forms of glioma in preclinical models through activity-regulated paracrine factors and direct neuron-to-glioma synapses. This synaptic integration of glioma into neural circuits is central to tumour growth and invasion. Thus, not only do neuron-oligodendroglial interactions modulate neural circuit structure and function in the healthy brain, but neuron-glioma interactions also have important roles in the pathogenesis of glial malignancies.© 2023. Springer Nature Limited.