ABSTRACT
Introduction: Increasing evidence has revealed that the Notch signalling pathway is one of the pivotal systems that mediate oligodendrocyte development. The Notch receptor is a type I transmembrane molecule that represents a novel cellular signalling paradigm, namely, regulated intramembrane proteolysis (RIP).
Method: The typical Notch ligands, such as Delta, Serrate/ Jagged and Lag2 (DSL), promote the formation of oligodendocyte precursor cells (OPCs) and maintain them in an uncommitted stage, thus retarding oligodendrocyte appearance in the central nervous system (CNS). Results: In contrast, our recent studies have revealed that F3/ contactin, a GPI-linked neural adhesion molecule, interacts with Notch and speeds up the generation and maturation of oligodendrocytes. Conclusions: Considering the distinct, albeit somewhat overlapping expression patterns of F3 and DSL in the CNS, the Notch receptor appears to function ligand-dependently during oligodendrocyte development. This multipotentiality may well designate the Notch receptor as one of the therapeutic targets that one can manoeuvre to treat demyelinating diseases, such as multiple sclerosis, that is characterised by chronic myelin degeneration.Oligodendrocytes (OLs) derived from the common neural progenitor cells in the central nervous system (CNS) ensheathe the nude axon to form the myelin that not only effects saltatory conduction but also protects and maintains the axonal structure. It is the last type of cells that appear in the CNS. The other 2 earlier types are neurons and astrocytes.
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