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{{BioPsy}}
   
[[Image:Oligodendrocyte.png|thumb|300px|Oligodendrocytes may be visualized by transfecting cells with [[green fluorescent protein]].]]
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{{Infobox Anatomy |
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Name = Oligodendrocyte |
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Latin = oligodendrocytus |
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GraySubject = |
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GrayPage = |
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Image = Oligodendrocyte.png |
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Caption = Oligodendrocyte |
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Image2 = Neuron with oligodendrocyte and myelin sheath.svg |
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Caption2 = Oligodendrocytes form the electrical insulation around the axons of [[Central nervous system|CNS]] nerve cells. |
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Precursor = |
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System = |
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Artery = |
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Vein = |
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Nerve = |
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Lymph = |
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MeshName = |
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MeshNumber = |
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Code = {{TerminologiaHistologica|2|00|06.2.01018}} |
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}}
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'''Oligodendrocytes''' (from [[Greek language|Greek]], meaning ''[[Cell (biology)|cells]] with a few branches''), or '''oligodendroglia''' (Greek, ''few tree glue''),<ref name="Ragheb_14">{{Harv|Ragheb|1999|p=14}}.</ref> are a type of [[brain]] cell. They are a variety of [[neuroglia]]. Their main functions are to provide support and to insulate the [[axon]]s (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 cell]]s in the [[peripheral nervous system]].) Oligodendrocytes do this by creating the [[myelin sheath]], which is 80% lipid and 20% protein.<ref name="CarlsonPhysiology">Carlson, Physiology of Behavior, 2010</ref> A single oligodendrocyte can extend its processes to 50 axons, wrapping approximately 1&nbsp;μm of myelin sheath around each axon; Schwann cells, on the other hand, can wrap around only 1 axon. Each oligodendrocyte forms one segment of myelin for several adjacent axons.<ref name="CarlsonPhysiology" />
   
'''Oligodendrocytes''' (from [[Greek language|Greek]] meaning ''few-branching cells''), or '''oligodendroglia''', are a variety of [[neuroglia]]. Their main function is the myelination of [[nerve cell]]s exclusively in the [[central nervous system]] of the higher [[vertebrates]] (in the [[peripheral nervous system]] the same function is carried out by [[Schwann cell]]s). A single oligodendrocyte can extend to about a dozen [[axon]]s, wrapping around approximately 1mm of each and forming the [[myelin sheath]].
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==Origin==
   
The [[nervous system]] (e.g., of humans) depends crucially on this sheath for insulation (decreased ion leakage and lower capacitance of the [[cell membrane]]), an overall increase in impulse speed (saltatory propagation of [[action potential]]s occurs in the PNS and the CNS at the nodes of Ranvier in between Schwann cells (of the PNS) and oligodendrocytes (of the CNS), and miniaturization (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).
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Oligodendroglia, types of [[glial cell]]s, arise during development from [[oligodendrocyte precursor cell]]s, which can be identified by their expression of a number of [[antigens]], including the [[ganglioside]] GD3,<ref>Curtis et al., 1988; LeVine and Goldman, 1988; Hardy and Reynolds, 1991; Levine et al., 1993</ref> the [[CSPG4|NG2 chondroitin sulfate proteoglycan]],<ref>Levine et al., 1993</ref> and the platelet-derived growth factor-alpha receptor subunit [[PDGF]]-alphaR.<ref>Pringle et al., 1992</ref> Most oligodendrocytes develop during embryogenesis and early postnatal life from restricted periventricular germinal regions.<ref>Vallstedt et al., 2004</ref>
   
Although they are part of the nervous system and very closely related to nerve cells, like all other glial cells the oligodendrocytes have a supporting role towards neurons and are probably not involved in signal propagation themselves.
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Oligodendroctyes 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.<ref>Richardson, W; D., Kessaris, Pringle, N (2006). "Oligodendrocyte wars". Nature Neuroscience Reviews. 1 7: 11-18</ref> They are the last cell type to be generated in the CNS.<ref>Thomas et al., Spatiotemporal development of oligodendrocytes in the embryonic brain., 2000</ref>
   
Diseases that result in injury to the oligodendroglial cells include demyelinating diseases such as [[multiple sclerosis]] and dysmyelinating diseases called [[leukodystrophy|leukodystrophies]]. 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 [[immunosuppression|immunocompromised]] patients. [[Tumor]]s of oligodendroglia are called oligodendrogliomas.
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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.<ref name="Fields">Fields, 2008</ref>
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Oligodendrocyte formation in the adult brain is associated with glial-restricted progenitors cells, known as oligodendrocyte progenitor cells (OPCs).<ref>Menn, et al., Origin of Oligodendrocytes in the Subventricular Zone of the Adult Brain, 2006</ref> [[Subventricular zone|SVZ]] cells migrate away from [[germinal]]<ref>Menn, et al., 2006</ref> zones to populate both developing white and gray matter, where they differentiate and mature into [[myelin]]-forming oligodendroglia.<ref>Hardy and Reynolds, 1991; Levison and Goldman, 1993</ref> However, it is not clear whether all oligodendroglial progenitors undergo this sequence of events. It has been suggested that some undergo [[apoptosis]] <ref>Barres et al., 1992</ref> and others fail to differentiate into mature oligodendroglia but persist as adult oligodendroglial progenitors.<ref>Wren et al., 1992</ref>
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==Function==
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[[File:Oligodendrocyte illustration.png|thumb|An oligodendrocyte seen [[myelin]]ating several axons.]]
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As part of the [[nervous system]], oligodendrocytes are closely related to nerve cells, and, like all other [[glial cell]]s, 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]].<ref>Sokol, 2009</ref> Myelin also increases impulse speed, as [[Saltatory conduction|saltatory propagation]] of [[action potential]]s occurs at the [[nodes of Ranvier]] in between [[Schwann cells]] (of the [[Peripheral nervous system|PNS]]) and oligodendrocytes (of the [[Central nervous system|CNS]]).
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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. 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.<ref name="Fields" />
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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.<ref>Baumann and Pham-Dinh, 2001</ref> Satellite oligodendrocytes are considered to be a part of the gray matter whereas myelinating oligodendrocytes are a part of the white matter.
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Myelination is an important component of intelligence. Neuroscientist Vincent J. Schmithorst found that there is a correlation with white matter and intelligence. People with greater white matter had higher IQ's.<ref name="Fields" /> 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.<ref>{{cite journal | author = Juraska J. M., Kopcik J. R. | year = 1988 | title = Sex and environmental influences on the size and ultrastructure of the rat corpus callosum | url = | journal = Brain Research | volume = 450 | issue = 1–2| pages = 1–8 | doi = 10.1016/0006-8993(88)91538-7 | pmid = 3401704 | ref = harv }}</ref>
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==Pathology==
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Diseases that result in injury to the oligodendroglial cells include demyelinating diseases such as [[multiple sclerosis]] and [[leukodystrophy|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. In cerebral palsy, spinal cord injury, stroke and possibly multiple sclerosis, oligodendrocytes are thought to be damaged by excessive release of the neurotransmitter glutamate.<ref name="Karadottiret">Káradóttir et al., 2007</ref> Damage has also been shown to be mediated by N-methyl-d-aspartate receptors.<ref name="Karadottiret" /> Oligodendrocyte dysfunction may also be implicated in the pathophysiology of schizophrenia and bipolar disorder.<ref>Tkachev et al., 2003</ref>
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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 [[immunosuppression|immunocompromised]] patients. [[Tumor]]s of oligodendroglia are called [[oligodendroglioma]]s. The chemotherapy agent [[Fluorouracil|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.<ref>[http://www.urmc.rochester.edu/biomedical-genetics/faculty/chemotherapy-induced-damage-to-cns.cfm "Chemotherapy-induced Damage to the CNS as a Precursor Cell Disease"] by Dr. Mark D. Noble, University of Rochester</ref>
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==See also==
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*[[2',3'-Cyclic-nucleotide 3'-phosphodiesterase]]
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== Notes ==
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{{reflist}}
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==References==
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<div class="references-small">
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*{{Cite journal|surname1=Baumann|given1=Nicole|last1=Baumann|surname2=Pham-Dinh|given2=Danielle|first1=N|year=2001|last2=Pham-Dinh|first2=D|title=Biology of Oligodendrocyte and Myelin in the Mammalian Central Nervous System|journal=Physiological Reviews|volume=18|issue=2|pages=871–927|url=http://physrev.physiology.org/cgi/content/full/81/2/871|accessdate=2007-07-13|pmid=11274346|ref=harv|postscript=<!-- Bot inserted parameter. Either remove it; or change its value to "." for the cite to end in a ".", as necessary. -->{{inconsistent citations}}}}
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</div>
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<div class="references-small">
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*{{Cite document|surname=Ragheb|given=Fadi|year=1999|title=The M3 Muscarinic Acetylcholine Receptor Mediates p42<sup>mapk</sup> Activation and c-fos mRNA Expression in Oligodendrocyte Progenitors|place=Ottawa|publisher=National Library of Canada|url=http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape9/PQDD_0025/MQ50862.pdf|accessdate=2006-03-07|ref=harv|postscript=<!-- Bot inserted parameter. Either remove it; or change its value to "." for the cite to end in a ".", as necessary. -->{{inconsistent citations}}}}
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</div>
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<div class="references-small">
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*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.&nbsp;115–141.
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</div>
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<div class="references-small">
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*{{cite journal | pmid = 13678875 | doi=10.1016/S0140-6736(03)14289-4 | volume=362 | issue=9386 | title=Oligodendrocyte dysfunction in schizophrenia and bipolar disorder | year=2003 | month=September | author=Tkachev D, Mimmack ML, Ryan MM, ''et al.'' | journal=Lancet | pages=798–805 | ref = harv}}
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</div>
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<div class="references-small">
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*{{cite journal|last=Káradóttir|first=R.|coauthors=D. Attwell|title=Neurotransmiter receptors in the life and death of oligodendrocytes|journal=Neuroscience|date=14|year=2007|month=April|volume=145|issue=4|pages=1426–1438|pmid=2173944|pmc=2173944|doi=10.1038/bjc.1990.391|ref=harv}}
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</div>
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<div class="references-small">
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*{{cite book|last=Carlson|first=Neil|title=Physiology of Behavior|year=2010|publisher=Allyn & Bacon|location=Boston, MA|isbn=0-205-66627-2|pages=38–39}}
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</div>
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<div class="references-small">
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*{{cite web|last=Sokol|first=Stacey|title=The Physiology and Pathophysiology of Multiple Sclerosis|url=http://mylifehealthandprosperity.com/index.php?option=com_content&view=article&id=65&Itemid=160|work=Multiple Sclerosis: Physiological Tutorial|accessdate=2012-04-29}}
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</div>
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<div class="references-small">
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*{{cite journal|last=Fields|first=Douglas|title=White Matter Matters|journal=Scientific American|date=18|year=2008|month=February|issue=March 2008|pages=54–61|url=http://www.scientificamerican.com/article.cfm?id=white-matter-matters|accessdate=2012-04-29|bibcode=2008SciAm.298c..54D|volume=298|doi=10.1038/scientificamerican0308-54|ref=harv}}
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</div>
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<div class="references-small">
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*{{cite journal|last=Menn|first=Benedicte|coauthors=Jose Manuel Garcia-Verdugo, Cynthia Yaschine, Oscar Gonzalez-Perez, David Rowitch, Arturo Alvarez-Buylla|title=Origin of Oligodendrocytes in the Subventricular Zone of the Adult Brain|journal=The Journal of Neuroscience|date=26|year=2006|month=July|volume=26|issue=30|pages=7907–7918|doi=10.1523/JNEUROSCI.1299-06.2006|url=http://www.jneurosci.org/content/26/30/7907.full|accessdate=2012-04-29|pmid=16870736|ref=harv}}
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</div>
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<div class="references-small">
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*{{cite journal|last=Vallstedt|first=A|coauthors=Klos JM, Ericson F|title=Multiple dorsoventral origins of oligodendrocyte generation in the spinal cord and hindbrain|journal=Neuron|date=6|year=2005|month=January|volume=45|series=1|pages=55–67|pmid=15629702|doi=10.1016/j.neuron.2004.12.026|issue=1|ref=harv}}
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</div>
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<div class="references-small">
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*{{cite journal|last=Thomas|first=JL|coauthors=Spassky N, Perez Villegas EM, Olivier C, Cobos I, Goujet-Zalc C, Martínez S, Zalc B.|title=Spatiotemporal development of oligodendrocytes in the embryonic brain|journal=Journal of Neuroscience Research|date=15|year=2000|month=February|volume=59|issue=4|pages=471–476|pmid=10679785|url=http://www.ncbi.nlm.nih.gov/pubmed/10679785|accessdate=2012-04-29|doi=10.1002/(SICI)1097-4547(20000215)59:4<471::AID-JNR1>3.0.CO;2-3|ref=harv}}
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</div>
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<div class="references-small">
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*{{cite journal|last=Richardson|first=W|coauthors=D., Kessaris, Pringle, N|title=Oligodendrocyte wars|journal=Nature Neuroscience Reviews|date=2006|volume=7|series=1|page=11–18|ref=harv|doi=10.1038/nrn1826}}
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</div>
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==External links==
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* The [[v:Topic:Neuroscience|Department of Neuroscience]] at [[v:|Wikiversity]]
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* [https://www.neuinfo.org/mynif/search.php?q=%22Oligodendrocyte%22&t=data&s=cover&b=0&r=20 NIF Search - Oligodendrocyte] via the [[Neuroscience Information Framework]]
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{{Nervous tissue}}
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{{Human cell types derived primarily from ectoderm}}
   
{{neuroscience-stub}}
 
 
[[Category:Glial cells]]
 
[[Category:Glial cells]]
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[[Category:Biology of bipolar disorder]]
   
[[nl:Oligodendrocyt]]
 
[[fr:Oligodendrocyte]]
 
[[de:Oligodendrozyt]]
 
 
{{enWP|Oligodendrocte}}
 
{{enWP|Oligodendrocte}}

Latest revision as of 16:36, October 2, 2013

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Oligodendrocyte
Oligodendrocyte
Oligodendrocyte
Latin oligodendrocytus
Gray's subject #
System
MeSH [1]
Oligodendrocytes form the electrical insulation around the axons of CNS nerve cells.

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 functions are to provide support and to insulate the 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.) 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 1 axon. Each oligodendrocyte forms one segment of myelin for several adjacent axons.[2]

OriginEdit

Oligodendroglia, types of glial cells, arise during development from oligodendrocyte precursor cells, which can be identified by their expression of a number of antigens, including the ganglioside GD3,[3] the NG2 chondroitin sulfate proteoglycan,[4] 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]

Oligodendroctyes 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]

Oligodendrocyte formation in the adult brain is associated with glial-restricted progenitors cells, known as oligodendrocyte progenitor cells (OPCs).[10] 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]

FunctionEdit

File:Oligodendrocyte illustration.png

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.[15] 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. 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 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.[16] 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 found 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.[17]

PathologyEdit

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. In cerebral palsy, spinal cord injury, stroke and possibly multiple sclerosis, oligodendrocytes are thought to be damaged by excessive release of the neurotransmitter glutamate.[18] Damage has also been shown to be mediated by N-methyl-d-aspartate receptors.[18] Oligodendrocyte dysfunction may also be implicated in the pathophysiology of schizophrenia and bipolar disorder.[19]

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.[20]

See alsoEdit

Notes Edit

  1. (Ragheb 1999, p. 14).
  2. 2.0 2.1 Carlson, Physiology of Behavior, 2010
  3. Curtis et al., 1988; LeVine and Goldman, 1988; Hardy and Reynolds, 1991; Levine et al., 1993
  4. Levine et al., 1993
  5. Pringle et al., 1992
  6. Vallstedt et al., 2004
  7. Richardson, W; D., Kessaris, Pringle, N (2006). "Oligodendrocyte wars". Nature Neuroscience Reviews. 1 7: 11-18
  8. Thomas et al., Spatiotemporal development of oligodendrocytes in the embryonic brain., 2000
  9. 9.0 9.1 9.2 Fields, 2008
  10. Menn, et al., Origin of Oligodendrocytes in the Subventricular Zone of the Adult Brain, 2006
  11. Menn, et al., 2006
  12. Hardy and Reynolds, 1991; Levison and Goldman, 1993
  13. Barres et al., 1992
  14. Wren et al., 1992
  15. Sokol, 2009
  16. Baumann and Pham-Dinh, 2001
  17. Juraska J. M., Kopcik J. R. (1988). Sex and environmental influences on the size and ultrastructure of the rat corpus callosum. Brain Research 450 (1–2): 1–8.
  18. 18.0 18.1 Káradóttir et al., 2007
  19. Tkachev et al., 2003
  20. "Chemotherapy-induced Damage to the CNS as a Precursor Cell Disease" by Dr. Mark D. Noble, University of Rochester

ReferencesEdit

  • 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, et al. (September 2003). Oligodendrocyte dysfunction in schizophrenia and bipolar disorder. Lancet 362 (9386): 798–805.
  • Káradóttir, R., D. Attwell (14). Neurotransmiter receptors in the life and death of oligodendrocytes. Neuroscience 145 (4): 1426–1438.
  • Carlson, Neil (2010). Physiology of Behavior, 38–39, Boston, MA: Allyn & Bacon.
  • Vallstedt, A, Klos JM, Ericson F (6). Multiple dorsoventral origins of oligodendrocyte generation in the spinal cord and hindbrain. Neuron 45 (1): 55–67.
  • Richardson, W, D., Kessaris, Pringle, N (2006). Oligodendrocyte wars. Nature Neuroscience Reviews 7.

External linksEdit


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