Voltage-operated Ca2+ and Na+ channels in the oligodendrocyte lineage

✍ Scribed by P.M. Paez; D. Fulton; C.S. Colwell; A.T. Campagnoni

• Publisher: John Wiley and Sons
• Year: 2009
• Tongue: English
• Weight: 213 KB
• Volume: 87
• Category: Article
• ISSN: 0360-4012
• DOI: 10.1002/jnr.21938

✦ Synopsis

Abstract

It is becoming increasingly clear that expression of Ca^2+^ and Na^+^ channels in the OL lineage is highly regulated and may be functionally related to different stages of development and myelination. Characterization of the mechanisms of voltage‐dependent Ca^2+^ and Na^+^ entry are important because changes in intracellular Ca^2+^ and Na^+^ are central to practically all cellular activities. In nonexcitable cells, voltage‐dependent Ca^2+^ influx plays a key role in several important processes, including proliferation, apoptosis, and cell migration. It has been demonstrated that Ca^2+^ signaling is essential in the development and functioning of OLs. For example, Ca^2+^ uptake is required for the initiation of myelination, and perturbation of Ca^2+^ homeostasis, e.g., overwhelming influxes of Ca^2+^, leads to demyelination. Although OL progenitor cell Na^+^ channels are present at a much lower density, their physiological properties appear to be indistinguishable from those recorded in neurons. Interestingly, recent data indicate that, as with neurons, some white matter OPCs possess the ability to generate Na^+^‐dependent action potentials. This Mini‐Review focuses on the mechanisms of Ca^2+^ and Na^+^ signaling in cells within the OL lineage mediated by voltage‐operated ion channels, with a particular focus on the relevance of these voltage‐dependent currents to oligodendroglial development, myelination, and demyelination. Overall, it is clear that cells in the OL lineage exhibit remarkable plasticity with regard to the expression of voltage‐gated Ca^2+^ and Na^+^ channels and that perturbation of Ca^2+^ and Na^+^ homeostasis likely plays an important role in the pathogenesis underlying demyelinating diseases. © 2008 Wiley‐Liss, Inc.