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Oligodendrocytes and Schwann cells
The major function of oligodendrocytes and Schwann cells is the formation of myelin. Myelin acts as an insulator of axonal segments and is a prerequisite for the high velocity of nerve conduction, of up to 200 m/second. The association of glial cells with axons is also found in invertebrates. Axon engulfing cells similar to the Remak cells of the vertebrates are found in most invertebrates. The formation of myelin by oligodendrocytes and Schwann cells are phylogenetically an invention of the vertebrates some 400 million years ago. All vertebrates except the jawless fish (hagfish and lampreys) have oligodendrocytes. The advent of myelin in evolution boosted the development of vertebrates and in particular their nervous system. Even most neuroscientists do not appreciate the importance of oligodendrocytes for the evolution of vertebrates. While it seems to be general knowledge that with the evolutionary development of the brain the number of neurones increases to up to 100 billion in human, it is not so evident that only due to myelin all these neurones can be interconnected in a complex fashion. This can be easily illustrated by the following  example. To increase the speed of nerve conduction one strategy is to form myelin, the other to increase the diameter of the axon. The giant axons in squid have a diameter of up to 1 mm and reach conduction velocities comparable to that of myelinated motor axons. The human optic nerve has about 1 million myelinated axons which conduct with a high speed.  A squid giant axon version with 1 million axons of 1 mm in diameter would amount to an axon diameter of 0.75 m. Taken into consideration that the human brain consists of up to 50% white matter it is evident that the high connectivity of the human brain would be impossible without the formation of myelin.
Morphology of oligodendrocytes
All white matter tracts contain oligodendrocytes to form myelin. Oligodendrocytes are, however, also found in gray matter. While oligodendrocytes are very well known as the myelin forming cells of the central nervous system there are also oligodendrocytes that are not directly connected to the myelin sheath. These satellite oligodendrocytes are preferentially found in gray matter and have so far unknown functions possibly serving to regulate ionic homeostasis similarly to astrocytes. Only the retina of rat, mouse and human is devoid of myelinating oligodendrocytes, the rabbit and chick retina are both partially myelinated. The myelin forming oligodendrocytes have several processes (up to 40) which connect to one myelin segment. Each of these segments is several hundred micrometers long and is also termed the internode. Segments are interrupted by structures known as node of Ranvier which spans for less than 1 micron. At the node, as compared to the internodal region, the axon is not enwrapped by myelin. The end of intermodal segment contains more cytoplasm and forms so called paranodal loop creating septate—like junctions with the axon. In addition, astrocyte processes contact the axonal membrane at the nodal region.
Like astrocytes oligodendrocytes are also interconnected by gap junctions formed by connexins. There are distinct connexin proteins for oligodendrocytes as compared to astrocytes. Mutations in the connexin proteins lead to hypomyelination and to human pathologies  such as leucodystrophies.
Development of oligodendrocytes
Myelin formation starts in rodents at about birth and is completed around 2 months after birth. In humans it starts during the second half of fetal life and begins in the spinal cord. Its peak activity is in the first year postnatally while it continues up to 20 years of age. It is generally noted that larger axons form thicker myelin. During development oligodendrocytes arise from precursors located in the subventricular zone such as the subventricular zone of the lateral ventricles for the cerebrum or the fourth ventricle for the cerebellum. In the spinal cord, oligodendrocytes originate from the ventral regions of the neural tube and in the optic nerve they migrate into the nerve from the third ventricle. It is the oligodendrocyte precursor cells which migrate to their destination where they then differentiate into the more mature oligodendrocytes. The proliferation of the oligodendrocyte progenitor cells is controlled by a number of growth factors released predominantly from neurons but also from astrocytes such as platelet derived growth factor (PDGF) or fibroblast growth factor (FGF). Moreover, an intrinsic clock seems to not only count cell division, but also senses time. Thus intrinsic mechanisms and the environment control the proper amount of oligodendrocytes required for myelination. Oligodendrocytes produced in excess (which occurs under normal conditions) are eliminated by apoptosis.
Oligodendrocyte progenitor cells, which can still give rise to astrocytes and oligodendrocytes are not only found during development but also exist in the mature brain being termed adult oligodendrocyte precursor cells. They are considered as a source for remyelination in demyelinating diseases such as multiple sclerosis. There are a number of distinct markers which help to identify these precursor cells such as the transcription factor Olig-2 or the proteoglycane NG2. These NG2 positive cells have recently attracted considerable attention. While they have the capacity to develop into astrocytes and oligodendrocytes, the main route seems to be confined to the oligodendrocyte lineage. These adult precursor cells seem to interact with axons. They express glutamate receptors and sense the activity of the axon, which releases glutamate in an activity dependent fashion. This seems to be a potential mechanism for how axons might control the differentiation of oligodendrocyte progenitor cells.
Schwann cells
Schwann cells are the cellular counterparts to oligodendrocytes in the peripheral nervous system. Similarly to oligodendrocytes they form the myelin sheath. In contrast to the oligodendrocyte each Schwann cell is associated with only one axonal segment. While the myelin structure formed by oligodendrocytes and Schwann cells has a similar ultrastructure, it is not composed of an identical set of proteins. While central and peripheral myelin share the basic protein myelin, the peripheral nervous system lacks myelin associated glycoprotein or proteolipid protein, but expresses the protein P0 and PMP22. During development, Schwann cells are derived from undifferentiated migrating neural crest cells. The immature Schwann cells produce either myelinating or non-myelinating Schwann cells. The latter loosely enwraps several axons without forming myelin.
Neuronal cell bodies in sensory sympathetic and parasympathetic ganglia are surrounded by flattened sheath like cells known as satellite cells. The axon terminals at a neuromuscular junction are also covered by specialized glial cells, namely the terminal glia.
The myelin sheaths
The myelin sheath is formed by an enwrappment of the axon by oligodendrocyte or Schwann cell processes. The intracellular compartment is very much compressed spanning only 30 Angström and appears in the electron microscope as a single line, called the major dense line. The outer surface of the lipid bilayer appears as a distinct line separated by the extracellular space. Therefore, this is defined as the double intraperiod line. Due to this immense compaction, myelin is purely hydrated and its dry mass contains about 70% lipids and 30% proteins. There are a number of highly specific proteins which are only found in myelin and are necessary for the formation of this structure. The major proteins of the central nervous system myelin are myelin associated glycoprotein (MAG), myelin basic protein (MBP), myelin oligodendrocyte glycoprotein (MOG), proteolipidprotein (PLP)/DM20 and PMP22. These proteins are exclusively produced by myelin-forming cells, namely oligodendrocytes in the central nervous system or by Schwann cells in the peripheral nervous system and thus serve as excellent markers for myelinating cells. Within the myelin layers, are kind of pathway which contain a cytoplasmic spacing named the Schmidt-Lantermann incisures. These provide trophic support for myelin.
Not all vertebrate axons are myelinated, but in general, axons larger than 1 micron are myelinated. Recent studies show that the axons provide a signal to the oligodendrocyte which determine the thickness of the myelin sheath. One important  signaling mechanism provided by the axon is via the growth factor neuregulin-1 which binds to ErbB receptor tyrosine kinases expressed by oligodendrocytes. A similar signaling mechanism also exists in Schwann cells. This interaction leads to a defined ratio between axonal diameter and axonal diameter plus myelin sheath, the so-called g-ratio which is usually between 0.6 to 0.7 .
It has long been speculated that myelinating cells do provide metabolic support to the axons. It can be speculated that glia derived glycolytic products such as pyruvate or lactate are released and taken up by the axon. This may be even more important for the peripheral nervous system since metabolites from the soma would have to be transported for distances of more than a meter in large animals.
Myelin enables saltatory nerve conduction
The node of Ranvier contains a high density of sodium channels, which allows what is known as saltatory conduction (from the latin word ´saltare´ which means ‘to jump’), namely the generation of action potentials only at the node. Thus the action potential is only triggered at the node, then spreads passively, and thus rapidly to the next node where the next action potential is generated. So the action potential jumps from node to node. This is not only faster, but consumes much less energy, since sodium ions accumulate only at the node and there need only to be transported back to the extracellular space due to the activity of the Na+/K+-ATPase. Before myelin formation the sodium channels are randomly distributed along the length of the axon. However, at the time of the glial ensheathment, sodium channels start to form loose clusters at the site, which later become the node of Ranvier. Subsequently, after formation of compact myelin, sodium channels disappear from the membrane underneath the myelin sheath and cluster only at the node. This clustering is promoted by protein interactions between the myelinating cell membrane and the axonal membrane involving cell adhesion molecules like gliomedin, neurofascin and NCAM. K+ channels are less stringently concentrated in the nodal region.
Myelinating cells and diseases
The most frequent disease involving oligodendrocytes is multiple sclerosis. It is caused by a loss of myelin in defined areas of brain and spinal cord and thus leads to an impairment of axonal conductance. Recovery can occur due to re-myelination but often relapses occur which lead to continuous neurodegeneration. The primary cause for the loss of oligodendrocytes is as yet unknown. It is evident that the demyelinated region contains inflammatory cells such as infiltrating lymphocytes and macrophages and activated microglia. These cells might potentiate or even initiate the damage cascade. Other inherited myelin disorders of the central nervous system are Pelizaeus-Merzbacher disease and Pelizaeus-Merzbacher-like diseases and other forms of leukodystrophies. Most of the genetically determined pathologies are associated with mutations in myelin proteins or connexins, the molecular entities forming gap junctions. Similarly to the central nervous system mutations in Schwann cell myelin or gap junction proteins lead to neuropathies such as the Charcot–Marie–Tooth disease. This makes it evident that peripheral myelin formation is also essential for the survival of vertebrates.

Adapted from: Kettenmann H.; Verkhratsky A. (2011) Neuroglia - Living Nerve Glue,  Fortschritte der Neurologie und Psychiatrie   79: 588-597