Abstract
Oligodendrocytes are the myelinating glia of the central nervous system. Myelination of axons allows rapid saltatory conduction of nerve impulses and contributes to axonal integrity. Devastating neurological deficits caused by demyelinating diseases, such as multiple sclerosis, illustrate well the importance of the process. In this review, we focus on the positive and negative interactions between oligodendrocytes, astrocytes, and microglia during developmental myelination and remyelination. Even though many lines of evidence support a crucial role for glia crosstalk during these processes, the nature of such interactions is often neglected when designing therapeutics for repair of demyelinated lesions. Understanding the cellular and molecular mechanisms underlying glial cell communication and how they influence oligodendrocyte differentiation and myelination is fundamental to uncover novel therapeutic strategies for myelin repair.
Highlights
Glial cells, neuroglia, or glia, in the adult mammalian central nervous system (CNS) comprise astrocytes, oligodendrocytes, and microglia
This study shows that oligodendrocyte progenitor cells (OPC) can modulate neuroinflammation and promote regeneration and are not simple target cells
The results showed that astrocyte-conditioned medium was more efficient in promoting
Summary
Neuroglia, or glia, in the adult mammalian central nervous system (CNS) comprise astrocytes, oligodendrocytes, and microglia. They are by far the most abundant cells in the nervous system. Astrocytes have star-shape morphology and are the most abundant CNS glial cell type They play essential functions in blood brain barrier maintenance, neuronal survival, and in synapse formation, strength, and turnover (Barres, 2008). First characterized by del Río-Hortega (1928), oligodendrocytes are the myelinating glia of the CNS (Nave and Werner, 2014) and their myelin sheaths enwrap axons to allow fast saltatory conduction of action potentials. This review discusses how in their active interplay, astrocytes and microglia can modulate oligodendrocyte homeostasis during myelination, demyelination and remyelination
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