Neuron with oligodendrocyte and myelin sheath.svg
Oligodendrocytes form the electrical insulation around the axons of CNS nerve cells.
Latin oligodendrocytus
Code TH H2.

Oligodendrocytes (from Greek, meaning cells with a few branches), or oligodendroglia (Greek, few tree glue),[1] are a type of brain cell. They are a variety of neuroglia. Their main function is the insulation of axons (the long projection of nerve cells) in the central nervous system (the brain and spinal cord) of some vertebrates. (The same function is performed by Schwann cells in the peripheral nervous system). A single oligodendrocyte can extend its processes to 50 axons, wrapping around approximately 1 μm of myelin sheath around each axon; Schwann cells, on the other hand, can wrap around only 1 axon.



Oligodendroglia arise during development from oligodendrocyte precursor cells, which can be identified by their expression of a number of antigens, including the ganglioside GD3,[2] the NG2 chondroitin sulfate proteoglycan,[3] and the platelet-derived growth factor-alpha receptor subunit PDGF-alphaR.[4] In the rat forebrain, the majority of oligodendroglial progenitors arise during late embryogenesis and early postnatal development from cells of the subventricular zones (SVZ) of the lateral ventricles. SVZ cells migrate away from germinal[disambiguation needed ] zones to populate both developing white and gray matter, where they differentiate and mature into myelin-forming oligodendroglia.[5] However, it is not clear whether all oligodendroglial progenitors undergo this sequence of events. It has been suggested that some undergo apoptosis [6] and others fail to differentiate into mature oligodendroglia but persist as adult oligodendroglial progenitors.[7]


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. 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). Oligodendrocytes provide the same functionality as the insulation on a household electrical wire (with the rather large difference that, while household electrical wires are in a non-conducting medium - air - the axons run in a solution of water and ions, which conducts electrical current well). 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. In contrast, Satellite oligodendrocytes are functionally distinct from most 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.[8]


Diseases that result in injury to the oligodendroglial cells include demyelinating diseases such as multiple sclerosis and leukodystrophies. Trauma to the body, e.g. spinal cord injury, can also cause demyelination. Cerebral palsy (periventricular leukomalacia) is caused by damage to developing oligodendrocytes in the brain areas around the cerebral ventricles. Spinal cord injury also causes damage to oligodendrocytes.[9] In cerebral palsy, spinal cord injury, stroke and possibly multiple sclerosis, oligodendrocytes are thought to be damaged by excessive release of the neurotransmitter glutamate.[citation needed] Oligodendrocyte dysfunction may also be implicated in the pathophysiology of schizophrenia and bipolar disorder.[10] 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.

See also


  1. ^ (Ragheb 1999, p. 14).
  2. ^ Curtis et al., 1988; LeVine and Goldman, 1988; Hardy and Reynolds, 1991; Levine et al., 1993
  3. ^ Levine et al., 1993
  4. ^ Pringle et al., 1992
  5. ^ Hardy and Reynolds, 1991; Levison and Goldman, 1993
  6. ^ Barres et al., 1992
  7. ^ Wren et al., 1992
  8. ^ Baumann and Pham-Dinh, 2001
  9. ^ Crowe; Bresnahan, J. C.; Shuman, S. L.; Masters, J. N.; Beattie, M. S. (1997). "Apoptosis and delayed degeneration after spinal cord injury in rats and monkeys". Nature medicine 3 (1): 73–76. doi:10.1038/nm0197-73. PMID 8986744.  edit
  10. ^ Tkachev et al., 2003


  • 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.
  • Tkachev D, Mimmack ML, Ryan MM, Wayland M, Freeman T, Jones PB, Starkey M, Webster MJ, Yolken RH, Bahn S. (2003). Oligodendrocyte dysfunction in schizophrenia and bipolar disorder. Lancet. 2003 Sep 6;362(9386):798-805.PMID: 13678875

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