An increasing number of studies connect neuronal activity with developmental myelination but how neuronal activity regulates remyelination has not been clarified. In this study, we induced the demyelination of the dorsal corticospinal tract (dCST) by a mild contusion spinal cord injury (SCI) on the T10 segment, and manipulated the neuronal activity of the primary motor cortex (M1) using chemogenetic viruses to induce activity and to suppress it. We found that oligodendrocyte precursor cell (OPC) proliferation and oligodendrocyte maturity following remyelination was strengthened after 4-week of neuronal activity stimulation. Furthermore, hindlimb motor function was also found to be improved. Vice versa, suppression of neuronal activity attenuated these effects. These results indicate that bidirectional regulation of neuronal activity can effectively modulate the development of oligodendrocyte lineage cells and the remyelination process. Neuronal activity supports the proliferation of OPCs, improves oligodendrocyte maturation and amplifies the axonal remyelination process, even though leads to better motor function recovery. Manipulation of neuronal activity in a non-invasive manner is therefore a promising avenue for exploration towards the treatment of central nervous system (CNS) demyelination diseases.

越来越多的研究将神经元活动与发育髓鞘形成联系起来，但尚未阐明神经元活动如何调节髓鞘再生。在这项研究中，我们通过 T10 段的轻度挫伤脊髓损伤 (SCI) 诱导背侧皮质脊髓束 (dCST) 脱髓鞘，并使用化学遗传病毒操纵初级运动皮层 (M1) 的神经元活动以诱导活动并压制它。我们发现，神经元活动刺激 4 周后，髓鞘再生后少突胶质细胞前体细胞 (OPC) 增殖和少突胶质细胞成熟得到加强。此外，还发现后肢运动功能得到改善。反之亦然，抑制神经元活动减弱了这些影响。这些结果表明，神经元活动的双向调节可以有效地调节少突胶质细胞谱系细胞的发育和髓鞘再生过程。神经元活动支持 OPCs 的增殖，改善少突胶质细胞成熟并放大轴突髓鞘再生过程，即使导致更好的运动功能恢复。因此，以非侵入性方式操纵神经元活动是探索治疗中枢神经系统 (CNS) 脱髓鞘疾病的有希望的途径。