Oligodendrocyte

You don't need to be Editor-In-Chief to add or edit content to WikiDoc. You can begin to add to or edit text on this WikiDoc page by clicking on the edit button at the top of this page. Next enter or edit the information that you would like to appear here. Once you are done editing, scroll down and click the Save page button at the bottom of the page.

(Redirected from Oligodendroglia)
Jump to: navigation, search

Please Take Over This Page and Apply to be Editor-In-Chief for this topic: There can be one or more than one Editor-In-Chief. You may also apply to be an Associate Editor-In-Chief of one of the subtopics below. Please mail us [1] to indicate your interest in serving either as an Editor-In-Chief of the entire topic or as an Associate Editor-In-Chief for a subtopic. Please be sure to attach your CV and or biographical sketch.

Oligodendrocyte

Oligodendrocyte

General Information
Tissue type Nervous
Cell type Neuroglia
Location Central nervous system
Role Myelination
Identification Robertson, 1899
Ultrastructure
Soma size 10–20μm
Unique organelles None
Unique feature Myelinating processes

Oligodendrocytes (from Greek literally meaning few tree cells), or oligodendroglia (Greek, few tree glue),[1] are a variety of neuroglia. Their main function is the myelination of axons exclusively in the central nervous system of the higher vertebrates, a function performed by Schwann cells in the peripheral nervous system. A single oligodendrocyte can extend to up to 50 axons, wrapping around approximately 1 mm of each and forming the myelin sheath.

Origin

Oligodendroglia arise during development from an oligodendrocyte precursor cell which can be identified by its expression of a number of antigens, including the ganglioside GD3 [1], the NG2 chondroitin sulfate proteoglycan [1], and the platelet derived growth factor-alpha receptor subunit PDGF-alphaR [1]. 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 these germinal zones to populate both developing white and gray matter, where they differentiate and mature into myelin-forming oligodendroglia [1]. However, it is not clear whether all oligodendroglial progenitors undergo this sequence of events. It has been suggested that some undergo apoptosis [1] and that some fail to differentiate into oligodendroglia but persist into maturity as adult oligodendroglial progenitors [1].

Function

The nervous system of mammals depends crucially on the myelin sheath for insulation as it results in decreased ion leakage and lower capacitance of the cell membrane. There is also an overall increase in 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 miniaturization occurs, whereby 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.

As part of the nervous system they are closely related to nerve cells and like all other glial cells the oligodendrocytes have a supporting role towards neurons. They are intimately involved in signal propagation, providing the same functionality as the insulation on a household electrical wire.

Satellite oligodendrocytes are functionally distinct from most oligodendrocytes. They are not attached to neurons and therefore do not serve an insulating role. They remain close to neurons and regulate the extracellular fluid.[1]

Pathology

Diseases that result in injury to the oligodendroglial cells include demyelinating diseases such as multiple sclerosis and leukodystrophies. 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. In cerebral palsy, spinal cord injury, stroke and possibly multiple sclerosis, oligodendrocytes are thought to be damaged by excessive release of the neurotransmitter glutamate. Oligodendrocyte dysfunction may also be implicated in the pathophysiology of schizophrenia and bipolar disorder [1]. Oligodendroglia are also susceptible to infection by the JC virus, which causes progressive multifocal leukoencephalopathy (PML), a condition which specifically affects white matter, typically in immunocompromised patients. Tumors of oligodendroglia are called oligodendrogliomas.

Notes

References

  • 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

de:Oligodendrozytfr:Oligodendrocyte he:אוליגודנדרוציטים nl:Oligodendrociet

WikiDoc Help Menu

Quick Start..

Editing basics

Advanced editing

Communicating your edits

Help Videos You Can Watch


Acknowledgement and Attribution Regarding Sources of Content

Some of the initial content on this page may be incorporated in part from copyleft sources in the public domain including wikis such as Wikipedia and AskDrWiki. Drug information for patients came from the The National Library of Medicine. Infectious disease information may have come from the Centers for Disease Control (CDC). Differential Diagnoses are drawn from clinicians as well as an amalgamation of 3 sources: 1.The Disease Database; 2. Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:3; 3. Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:7 .

Personal tools