Are electrophysiological and oligodendrocyte alterations an element in the development of multiple sclerosis at the same time as or before the immune response?

• Published in: International journal of neuroscience 2021-12, Vol.131 (12), p.1221-1230
• Main Authors: Ortiz, Genaro Gabriel, Mireles-Ramírez, Mario A., Pacheco-Moisés, Fermín P., Ramírez-Jirano, Luis J., Bitzer-Quintero, Oscar K., Delgado-Lara, Daniela L. C., Flores-Alvarado, L. Javier, Mora-Navarro, Miriam A., Huerta, Miguel, Torres-Mendoza, Blanca M. G.
• Format: Article
• Language: English
• Subjects: Animals; Electrophysiological Phenomena - immunology; Electrophysiological Phenomena - physiology; Electrophysiology; Humans; immune response; Immunity - immunology; Immunity - physiology; multiple sclerosis; Multiple Sclerosis - immunology; Multiple Sclerosis - metabolism; Multiple Sclerosis - pathology; Multiple Sclerosis - physiopathology; oligodendrocyte; Oligodendroglia - immunology; Oligodendroglia - metabolism; Oligodendroglia - pathology; Oligodendroglia - physiology
• ISSN: 0020-7454; 1563-5279; 1543-5245
• DOI: 10.1080/00207454.2020.1786087

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.