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Physiol. Rev. 81: 871-927, 2001;
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Physiological Reviews, Vol. 81, No. 2, April 2001, pp. 871-927
Copyright ©2001 by the American Physiological Society

Biology of Oligodendrocyte and Myelin in the Mammalian Central Nervous System

Nicole Baumann and Danielle Pham-Dinh

Institut National de la Santé et de la Recherche Médicale U. 495, Biology of Neuron-Glia Interactions, Salpêtrière Hospital, and Neurogenetic Laboratory, Neuroscience Institute, Unité Mixte de Recherche 7624 Centre National de la Recherche Scientifique, University Paris, Paris, France

Baumann, Nicole and Danielle Pham-Dinh. Biology of Oligodendrocyte and Myelin in the Mammalian Central Nervous System. Physiol. Rev. 81: 871-927, 2001.Oligodendrocytes, the myelin-forming cells of the central nervous system (CNS), and astrocytes constitute macroglia. This review deals with the recent progress related to the origin and differentiation of the oligodendrocytes, their relationships to other neural cells, and functional neuroglial interactions under physiological conditions and in demyelinating diseases. One of the problems in studies of the CNS is to find components, i.e., markers, for the identification of the different cells, in intact tissues or cultures. In recent years, specific biochemical, immunological, and molecular markers have been identified. Many components specific to differentiating oligodendrocytes and to myelin are now available to aid their study. Transgenic mice and spontaneous mutants have led to a better understanding of the targets of specific dys- or demyelinating diseases. The best examples are the studies concerning the effects of the mutations affecting the most abundant protein in the central nervous myelin, the proteolipid protein, which lead to dysmyelinating diseases in animals and human (jimpy mutation and Pelizaeus-Merzbacher disease or spastic paraplegia, respectively). Oligodendrocytes, as astrocytes, are able to respond to changes in the cellular and extracellular environment, possibly in relation to a glial network. There is also a remarkable plasticity of the oligodendrocyte lineage, even in the adult with a certain potentiality for myelin repair after experimental demyelination or human diseases.




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