Institute of Pharmacology and Toxicology, University of Zurich, Zurich, Switzerland; Neuroscience Center Zurich, University and ETH Zurich, Zurich, Switzerland.
Max Planck Institute of Experimental Medicine, Department of Neurogenetics, Göttingen, Germany.
Curr Opin Neurobiol. 2017 Dec;47:104-112. doi: 10.1016/j.conb.2017.09.013. Epub 2017 Nov 20.
Myelinating glial cells are well-known to insulate axons and to speed up action potential propagation. Through adjustments in the axonal coverage with myelin, myelin sheath thickness and possibly nodal/internode length oligodendrocytes are involved in fine-tuning the brain's computational power throughout life. Be it motor skill learning or social behaviors in higher vertebrates, proper myelination is critical in shaping brain functions. Neurons rely on their myelinating partners not only for setting conduction speed, but also for regulating the ionic environment and fueling their energy demands with metabolites. Also, long-term axonal integrity and neuronal survival are maintained by oligodendrocytes and loss of this well-coordinated axon-glial interplay contributes to neuropsychiatric diseases. Better insight into how myelination and oligodendrocyte functions are constantly fine-tuned in the adult CNS, which includes sensing of neuronal activity and adjusting glial metabolic support, will be critical for understanding higher brain functions and cognitive decline associated with myelin abnormalities in the aging brain.
少突胶质细胞是众所周知的轴突绝缘和加快动作电位的传播。通过调整有髓轴突的覆盖范围、髓鞘厚度和可能的节间/节段长度，少突胶质细胞参与了一生中大脑计算能力的微调。无论是运动技能学习还是高等脊椎动物的社会行为，适当的髓鞘形成对于塑造大脑功能至关重要。神经元不仅依靠其髓鞘形成伙伴来设置传导速度，还依靠它们来调节离子环境，并为其代谢物提供能量需求。此外，长期的轴突完整性和神经元存活是由少突胶质细胞维持的，而这种协调良好的轴突-胶质相互作用的丧失导致神经精神疾病。更好地了解髓鞘形成和少突胶质细胞功能如何在成人中枢神经系统中不断微调，包括对神经元活动的感知和调整胶质代谢支持，对于理解与衰老大脑中髓鞘异常相关的大脑高级功能和认知能力下降至关重要。
