Abstract

Efficient communication between the glial cells and neurons is a bi-directional process that is essential for conserving normal functioning in the central nervous system (CNS). Neurons dynamically regulate other brain cells in the healthy brain, yet little is known about the first pathways involving oligodendrocytes and neurons. Oligodendrocytes are the myelin-forming cells in the CNS that are needed for the propagation of action potentials along axons and additionally serve to support neurons by neurotrophic factors (NFTs). In demyelinating diseases, like multiple sclerosis (MS), oligodendrocytes are thought to be the victims. Axonal damage begins early and remains silent for years, and neurological disability develops when a threshold of axonal loss is reached, and the compensatory mechanisms are depleted. Three hypotheses have been proposed to explain axonal damage: 1) the damage is caused by an inflammatory process; 2) there is an excessive accumulation of intra-axonal calcium levels; and, 3) demyelinated axons evolve to a degenerative process resulting from the lack of trophic support provided by myelin or myelin-forming cells. Although MS was traditionally considered to be a white matter disease, the demyelination process also occurs in the cerebral cortex. Recent data supports the notion that initial response is triggered by CNS injury. Thus, the understanding of the role of neuron-glial neurophysiology would help provide us with further explanations. We should take in account the suggestion that MS is in part an autoimmune disease that involves genetic and environmental factors, and the pathological response leads to demyelination, axonal loss and inflammatory infiltrates.

摘要

神经胶质细胞和神经元之间的有效交流是一个双向过程，对于保持中枢神经系统 (CNS) 的正常功能至关重要。神经元动态调节健康大脑中的其他脑细胞，但对涉及少突胶质细胞和神经元的第一条通路知之甚少。少突胶质细胞是 CNS 中的髓鞘形成细胞，它们是沿轴突传播动作电位所需的，另外还通过神经营养因子 (NFT) 支持神经元。在多发性硬化症 (MS) 等脱髓鞘疾病中，少突胶质细胞被认为是受害者。轴突损伤很早就开始并保持沉默多年，当达到轴突损失阈值并且代偿机制耗尽时，就会出现神经功能障碍。已经提出了三个假设来解释轴突损伤：1）损伤是由炎症过程引起的；2）轴突内钙水平过度积累；并且，3) 脱髓鞘轴突由于缺乏髓磷脂或髓磷脂形成细胞提供的营养支持而演变为退化过程。虽然 MS 传统上被认为是一种白质疾病，但脱髓鞘过程也发生在大脑皮层。最近的数据支持初始反应是由 CNS 损伤触发的概念。因此，了解神经胶质神经生理学的作用将有助于为我们提供进一步的解释。我们应该考虑到 MS 部分是一种自身免疫性疾病，涉及遗传和环境因素，病理反应导致脱髓鞘，