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髓鞘和少突胶质细胞在轴突能量代谢中的作用。

The role of myelin and oligodendrocytes in axonal energy metabolism.

机构信息

Max Planck Institute of Experimental Medicine, Department of Neurogenetics, Göttingen, Germany.

出版信息

Curr Opin Neurobiol. 2013 Dec;23(6):1065-72. doi: 10.1016/j.conb.2013.09.008. Epub 2013 Oct 4.

DOI:10.1016/j.conb.2013.09.008
PMID:24094633
Abstract

In vertebrates, the myelination of long axons by oligodendrocytes and Schwann cells enables rapid impulse propagation. However, myelin sheaths are not only passive insulators. Oligodendrocytes are also known to support axonal functions and long-term integrity. Some of the underlying mechanisms have now been identified. It could be shown that oligodendrocytes can survive in vivo by aerobic glycolysis. Myelinating oligodendrocytes release lactate through the monocarboxylate transporter MCT1. Lactate is then utilized by axons for mitochondrial ATP generation. Studying axo-glial signalling and energy metabolism will lead to a better understanding of neurodegenerative diseases, in which axonal energy metabolism fails. These include neurological disorders as diverse as multiple sclerosis, leukodystrophies, and amyotrophic lateral sclerosis.

摘要

在脊椎动物中,少突胶质细胞和施万细胞对长轴突的髓鞘形成使冲动得以快速传播。然而,髓鞘不仅是被动的绝缘体。少突胶质细胞还被认为能够支持轴突的功能和长期完整性。现在已经确定了一些潜在的机制。研究表明,少突胶质细胞可以通过有氧糖酵解在体内存活。少突胶质细胞通过单羧酸转运蛋白 MCT1 释放乳酸盐。然后,轴突利用乳酸盐进行线粒体 ATP 的产生。研究轴突-胶质细胞信号传递和能量代谢将有助于更好地理解神经退行性疾病,其中轴突的能量代谢失败。这些疾病包括多发性硬化症、白质营养不良症和肌萎缩性侧索硬化症等多种神经紊乱。

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