BioLegend Oligodendrocytes
Background   Featured Products   Role in Disease
Oligodendrocytes (ODs) are a type of glial cell that produce myelin sheath to allow for the insulation of segments of neuronal axons. This enables high velocity signal transduction, which is essential for the propagation of action potentials along the axon. ODs also contribute to neuroplasticity and provide trophic support to neurons. Each OD can extend its processes to multiple axons and has a great capacity to rapidly renew its myelin sheath. As a result, ODs have a high metabolic rate and are highly vulnerable to oxidative stress. The latter is also partly due to ODs having relatively low levels of anti-oxidative enzymes. As a consequence, ODs are highly susceptible to proinflammatory molecules produced during inflammation and respond by producing low quality myelin. This in turn, may lead to the loss of OD-neuron connections and axon degeneration. Myelin basic protein (MBP), myelin CNPase, and CD140a are specific markers that allow identification of oligodendrocytes.

OD development and maturation can be divided into four stages in mice. During embryonic development, neural stem cells (NSCs) give rise to oligodendrocyte precursor cells (OPCs). OPCs then proliferate and migrate to different regions of the brain, and subsequently differentiate into pre-oligodendrocytes (pre-OLs). These cells can further mature into myelinating oligodendrocytes. OPCs continue to proliferate and differentiate into ODs in the adult brain. Each stage in the development and maturation of ODs can be identified using a panel of markers.
A2B5A2B5Adenomatous polyposis coli (APC)CNP
CNPCNPCNPMAG
NG2NG2GalCMOG
Nkx2.2Nkx2.2MBPO4
Olig1/2O4O4Olig1/2
Sox-10Olig1/2Olig1/2Sox-10
PDGFRα (CD140a)Sox-10Sox-10 
VimentinPDGFRα (CD140a)  
 Vimentin  
Schematic representation demonstrating morphological alteration and antigenic marker expression in each developmental stage in OD maturation.
References
1. Zuchero JB and Barres BA. 2013. Curr. Opin. Neurobiol. 23:914. PubMed
2. Mitew S, et al. 2014. Neuroscience. 12:29. PubMed
3. Traiffort E, et al. 2016. J. Dev. Biol. 4 :28. PubMed
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