World Library  
Flag as Inappropriate
Email this Article


Article Id: WHEBN0000383763
Reproduction Date:

Title: Oligodendrocyte  
Author: World Heritage Encyclopedia
Language: English
Subject: Pathology of multiple sclerosis, Sulfatide, Myelin, Glioblast, Axon
Collection: Biology of Bipolar Disorder, Glial Cells
Publisher: World Heritage Encyclopedia


Oligodendrocytes form the electrical insulation around the axons of CNS nerve cells.
Latin oligodendrocytus
Code TH H2.
Anatomical terminology

Oligodendrocytes (from Greek, meaning cells with a few branches), or oligodendroglia (Greek, few tree glue),[1] are a type of neuroglia. Their main functions are to provide support and insulation to axons in the central nervous system of some vertebrates, equivalent to the function performed by Schwann cells in the peripheral nervous system. Oligodendrocytes do this by creating the myelin sheath, which is 80% lipid and 20% protein.[2] A single oligodendrocyte can extend its processes to 50 axons, wrapping approximately 1 μm of myelin sheath around each axon; Schwann cells, on the other hand, can wrap around only one axon. Each oligodendrocyte forms one segment of myelin for several adjacent axons.[2]


  • Origin 1
  • Function 2
  • Pathology 3
  • See also 4
  • Notes 5
  • References 6
  • External links 7


Oligodendroglia, types of glial cells, arise during development from oligodendrocyte precursor cells,[3] which can be identified by their expression of a number of antigens, including the ganglioside GD3,[4] the NG2 chondroitin sulfate proteoglycan, and the platelet-derived growth factor-alpha receptor subunit (PDGF-alphaR).[5] Most oligodendrocytes develop during embryogenesis and early postnatal life from restricted periventricular germinal regions.[6]

Oligodendrocytes are found only in the central nervous system which comprises the brain and spinal cord. These cells were originally thought to have been produced in the ventral neural tube; however, research now shows oligodendrocytes originate from the ventral ventricular zone of the embryonic spinal cord and possibly have some concentrations in the forebrain.[7] They are the last cell type to be generated in the CNS.[8]

Myelination is only prevalent in a few brain regions at birth and continues into adulthood. The entire process is not complete until about 25–30 years of age.[9]

The group of Prof. Arturo Alvarez-Buylla[10] demonstrate that oligodendrocyte formation in the adult brain is associated with glial-restricted progenitor cells, known as oligodendrocyte progenitor cells (OPCs).[11] SVZ cells migrate away from germinal[11] zones to populate both developing white and gray matter, where they differentiate and mature into myelin-forming oligodendroglia.[12] However, it is not clear whether all oligodendroglial progenitors undergo this sequence of events. It has been suggested that some undergo apoptosis [13] and others fail to differentiate into mature oligodendroglia but persist as adult oligodendroglial progenitors.[14] Remarkably, oligodendrocyte population originated in the subventricular zona can be dramatically expanded by administering epidermal growth factor (EGF).[15][16]


An oligodendrocyte seen myelinating several axons.

As part of the nervous system, oligodendrocytes are closely related to nerve cells, and, like all other glial cells, oligodendrocytes provide a supporting role for neurons. In addition, the nervous system of mammals depends crucially on myelin sheaths, which reduce ion leakage and decrease the capacitance of the cell membrane.[17] Myelin also increases impulse speed, as saltatory propagation of action potentials occurs at the nodes of Ranvier in between Schwann cells (of the PNS) and oligodendrocytes (of the CNS). Furthermore, impulse speed of myelinated axons increases linearly with the axon diameter, whereas the impulse speed of unmyelinated cells increases only with the square root of the diameter. The insulation must be proportional to the diameter of the fiber inside. The optimal ratio of axon diameter divided by the total fiber diameter (which includes the myelin) is 0.6.[9]

In contrast, satellite oligodendrocytes are functionally distinct from other oligodendrocytes. They are not attached to neurons and, therefore, do not serve an insulating role. They remain apposed to neurons and regulate the extracellular fluid.[18] Satellite oligodendrocytes are considered to be a part of the gray matter whereas myelinating oligodendrocytes are a part of the white matter.

Myelination is an important component of intelligence. Neuroscientist Vincent J. Schmithorst suggests that there is a correlation with white matter and intelligence. People with greater white matter had higher IQ's.[9] A study done with rats by Janice M. Juraska showed that rats that were raised in an enriched environment had more myelination in their corpus callosum.[19]

Oligodendrocytes in rat cerebellum stained with antibody to myelin basic protein in red and for DNA in blue. Two oligodendrocyte cell bodies are clearly visible as well as several myelinated axons. These are hollow tubes and so appear as "tramlines" in this confocal image. Most of the DNA is in the nuclei of cerebellum granule cells, which are small interneurons. Image and antibody stain from EnCor Biotechnology Inc.


Diseases that result in injury to the oligodendroglial cells include demyelinating diseases such as multiple sclerosis and various leukodystrophies. Trauma to the body, e.g. spinal cord injury, can also cause demyelination. Cerebral palsy, (sometimes developing from periventricular leukomalacia), is largely congenital and caused by damage to the newly forming brain. In cerebral palsy, spinal cord injury, stroke and possibly multiple sclerosis, oligodendrocytes are thought to be damaged by excessive release of the neurotransmitter, glutamate.[20] Damage has also been shown to be mediated by N-methyl-D-aspartate receptors.[20] Oligodendrocyte dysfunction may also be implicated in the pathophysiology of schizophrenia and bipolar disorder.[21]

Oligodendroglia are also susceptible to infection by the JC virus, which causes progressive multifocal leukoencephalopathy (PML), a condition that specifically affects white matter, typically in immunocompromised patients. Tumors of oligodendroglia are called oligodendrogliomas. The chemotherapy agent Fluorouracil (5-FU) causes damage to the oligodendrocytes in mice, leading to both acute central nervous system (CNS) damage and progressively worsening delayed degeneration of the CNS.[22] [23]

See also


  1. ^ (Ragheb 1999, p. 14).
  2. ^ a b Carlson, Physiology of Behavior, 2010
  3. ^ Cameron-Curry, Patrizia; Le Douarin, Nicole M. (December 1995). "Oligodendrocyte precursors originate from both the dorsal and the ventral parts of the spinal cord". Neuron 15 (6): 1299–1310.  
  4. ^ Curtis et al., 1988; LeVine and Goldman, 1988; Hardy and Reynolds, 1991
  5. ^ Pringle, NP; Mudhar, HS; Collarini, EJ; Richardson, WD (Jun 1992). "PDGF receptors in the rat CNS: during late neurogenesis, PDGF alpha-receptor expression appears to be restricted to glial cells of the oligodendrocyte lineage." (PDF). Development (Cambridge, England) 115 (2): 535–51.  
  6. ^ Vallstedt et al., 2004
  7. ^ Richardson, WD; Kessaris, N; Pringle, N (Jan 2006). "Oligodendrocyte wars.". Nature reviews. Neuroscience 7 (1): 11–8.  
  8. ^ Thomas, JL; Spassky, N; Perez Villegas, EM; Olivier, C; Cobos, I; Goujet-Zalc, C; Martínez, S; Zalc, B (Feb 15, 2000). "Spatiotemporal development of oligodendrocytes in the embryonic brain". Journal of neuroscience research 59 (4): 471–6.  
  9. ^ a b c Fields, 2008
  10. ^ Gonzalez-Perez, O; Alvarez-Buylla, A (2011). "Oligodendrogenesis in the subventricular zone and the role of epidermal growth factor". Brain Research Reviews 67 (1–2): 147–56.  
  11. ^ a b Menn, B; Garcia-Verdugo, JM; Yaschine, C; Gonzalez-Perez, O; Rowitch, D; Alvarez-Buylla, A (Jul 26, 2006). "Origin of oligodendrocytes in the subventricular zone of the adult brain.". The Journal of neuroscience : the official journal of the Society for Neuroscience 26 (30): 7907–18.  
  12. ^ Hardy and Reynolds, 1991; Levison and Goldman, 1993
  13. ^ Barres et al., 1992
  14. ^ Wren et al., 1992
  15. ^ Gonzalez-Perez, O, B; Romero-Rodriguez, R,; Soriano-Navarro, M; Garcia-Verdugo, JM; Alvarez-Buylla, A (2009). "Epidermal growth factor induces the progeny of subventricular zone type B cells to migrate and differentiate into oligodendrocytes". Stem Cells 27 (8): 2032–43.  
  16. ^ Gonzalez-Perez, O, B; Alvarez-Buylla, A (Jun 24, 2011). "Oligodendrogenesis in the subventricular zone and the role of epidermal growth factor". Brain Research Reviews 67 (1–2): 147–56.  
  17. ^ Sokol, 2009
  18. ^ Baumann and Pham-Dinh, 2001
  19. ^ Juraska J. M., Kopcik J. R.; Kopcik (1988). "Sex and environmental influences on the size and ultrastructure of the rat corpus callosum". Brain Research 450 (1–2): 1–8.  
  20. ^ a b Káradóttir et al., 2007
  21. ^ Tkachev et al., 2003
  22. ^ "Chemotherapy-induced Damage to the CNS as a Precursor Cell Disease" by Dr. Mark D. Noble, University of Rochester
  23. ^ Han, R; Yang, Y. M.; Dietrich, J; Luebke, A; Mayer-Pröschel, M; Noble, M (2008). "Systemic 5-fluorouracil treatment causes a syndrome of delayed myelin destruction in the central nervous system". Journal of Biology 7 (4): 12.  


  • Baumann, Nicole; Pham-Dinh, Danielle (2001). "Biology of Oligodendrocyte and Myelin in the Mammalian Central Nervous System". Physiological Reviews 18 (2): 871–927.  
  • Ragheb, Fadi (1999). Activation and c-fos mRNA Expression in Oligodendrocyte Progenitors"mapk"The M3 Muscarinic Acetylcholine Receptor Mediates p42 (PDF). Ottawa: National Library of Canada. Retrieved 2006-03-07 
  • Raine, C.S. (1991). Oligodendrocytes and central nervous system myelin. In Textbook of Neuropathology, second edition, R.L. Davis and D.M. Robertson, eds. (Baltimore, Maryland: Williams and Wilkins), pp. 115–141.
  • Káradóttir, R.; D. Attwell (14 April 2007). "Neurotransmiter receptors in the life and death of oligodendrocytes". Neuroscience 145 (4): 1426–1438.  
  • Carlson, Neil (2010). Physiology of Behavior. Boston, MA: Allyn & Bacon. pp. 38–39.  
  • Sokol, Stacey. "The Physiology and Pathophysiology of Multiple Sclerosis". Multiple Sclerosis: Physiological Tutorial. Retrieved 2012-04-29. 
  • Fields, Douglas (18 February 2008). "White Matter Matters". Scientific American 298 (March 2008): 54–61.  
  • Menn, Benedicte;  
  • Gonzalez-Perez, O, B; Romero-Rodriguez, R,; Soriano-Navarro, M; Garcia-Verdugo, JM; Alvarez-Buylla, A (2009). "Epidermal growth factor induces the progeny of subventricular zone type B cells to migrate and differentiate into oligodendrocytes.". Stem Cells 27 (8): 2032–43.  
  • Vallstedt, A; Klos JM, Ericson F (6 January 2005). "Multiple dorsoventral origins of oligodendrocyte generation in the spinal cord and hindbrain". Neuron. 1 45 (1): 55–67.  
  • Thomas, JL; Spassky N, Perez Villegas EM, Olivier C, Cobos I, Goujet-Zalc C, Martínez S, Zalc B. (15 February 2000). "Spatiotemporal development of oligodendrocytes in the embryonic brain". Journal of Neuroscience Research 59 (4): 471–476.  
  • Richardson, W; D., Kessaris, Pringle, N (2006). "Oligodendrocyte wars". Nature Neuroscience Reviews. 1 7 (1): 11–18.  

External links

This article was sourced from Creative Commons Attribution-ShareAlike License; additional terms may apply. World Heritage Encyclopedia content is assembled from numerous content providers, Open Access Publishing, and in compliance with The Fair Access to Science and Technology Research Act (FASTR), Wikimedia Foundation, Inc., Public Library of Science, The Encyclopedia of Life, Open Book Publishers (OBP), PubMed, U.S. National Library of Medicine, National Center for Biotechnology Information, U.S. National Library of Medicine, National Institutes of Health (NIH), U.S. Department of Health & Human Services, and, which sources content from all federal, state, local, tribal, and territorial government publication portals (.gov, .mil, .edu). Funding for and content contributors is made possible from the U.S. Congress, E-Government Act of 2002.
Crowd sourced content that is contributed to World Heritage Encyclopedia is peer reviewed and edited by our editorial staff to ensure quality scholarly research articles.
By using this site, you agree to the Terms of Use and Privacy Policy. World Heritage Encyclopedia™ is a registered trademark of the World Public Library Association, a non-profit organization.

Copyright © World Library Foundation. All rights reserved. eBooks from Project Gutenberg are sponsored by the World Library Foundation,
a 501c(4) Member's Support Non-Profit Organization, and is NOT affiliated with any governmental agency or department.