Editing Myelin (section)

== Function ==
{{Main|Saltatory conduction}}
[[File:Saltatory Conduction.gif|thumb|Action potential propagation in myelinated neurons is faster than in unmyelinated neurons because of [[saltatory conduction]].]]

The main purpose of myelin is to increase the speed at which electrical impulses (known as [[action potential]]s) propagate along the myelinated fiber. In unmyelinated fibers, action potentials travel as continuous waves, but, in myelinated fibers, they "hop" or propagate by [[saltatory conduction]]. The latter is markedly faster than the former, at least for axons over a certain diameter. Myelin decreases [[capacitance]] and increases [[electrical resistance]] across the axonal membrane (the [[axolemma]]). It has been suggested that myelin permits larger body size by maintaining agile communication between distant body parts.<ref name="Daniel">{{cite journal|vauthors=Hartline DK|title=What is myelin?|journal=Neuron Glia Biology|volume=4|issue=2|pages=153–63|date=May 2008|pmid=19737435|doi=10.1017/S1740925X09990263 |s2cid=33164806}}</ref>

Myelinated fibers lack [[voltage-gated sodium channels]] along the myelinated internodes, exposing them only at the [[nodes of Ranvier]]. Here, they are highly abundant and densely packed.<ref name="Saladin, Kenneth S. 2012">{{cite book|last=Saladin|first=Kenneth S.|name-list-style=vanc|title=Anatomy & physiology: the unity of form and function|edition=6th|location=New York|publisher=McGraw-Hill|date=2012 }}{{page needed|date=July 2018}}</ref> Positively charged sodium [[ion]]s can enter the axon through these voltage-gated channels, leading to [[depolarisation]] of the membrane potential at the node of Ranvier. The [[resting membrane potential]] is then rapidly restored due to positively charged potassium ions leaving the axon through [[potassium channels]]. The sodium ions inside the axon then diffuse rapidly through the axoplasm (axonal [[cytoplasm]]), to the adjacent myelinated internode and ultimately to the next ([[distal]]) node of Ranvier, triggering the opening of the voltage gated sodium channels and entry of sodium ions at this site. Although the sodium ions diffuse through the axoplasm rapidly, [[diffusion]] is decremental by nature, thus nodes of Ranvier have to be (relatively) closely spaced, to secure action potential propagation.<ref>{{cite book|vauthors=Raine CS|veditors=Siegel GJ, Agranoff BW, Albers RW, Fisher SK, Uhler MD|chapter=Characteristics of Neuroglia|title=Basic Neurochemistry: Molecular, Cellular and Medical Aspects|edition=6th|location=Philadelphia|publisher=Lippincott-Raven|year=1999|chapter-url=https://www.ncbi.nlm.nih.gov/books/NBK28217/ }}</ref> The action potential "recharges" at consecutive nodes of Ranvier as the axolemmal [[membrane potential]] depolarises to approximately +35 mV.<ref name="Saladin, Kenneth S. 2012"/> Along the myelinated internode, energy-dependent sodium/potassium pumps pump the sodium ions back out of the axon and potassium ions back into the axon to restore the balance of ions between the intracellular (inside the cell, i.e. axon in this case) and extracellular (outside the cell) fluids.

Whilst the role of myelin as an "axonal insulator" is well-established, other functions of myelinating cells are less well known or only recently established. The myelinating cell "sculpts" the underlying axon by promoting the [[phosphorylation]] of [[neurofilaments]], thus increasing the diameter or thickness of the axon at the internodal regions; helps cluster molecules on the axolemma (such as voltage-gated sodium channels) at the node of Ranvier;<ref>{{cite journal|vauthors=Brivio V, Faivre-Sarrailh C, Peles E, Sherman DL, Brophy PJ|title=Assembly of CNS Nodes of Ranvier in Myelinated Nerves Is Promoted by the Axon Cytoskeleton|journal=Current Biology|volume=27|issue=7|pages=1068–73|date=April 2017|pmid=28318976|pmc=5387178|doi=10.1016/j.cub.2017.01.025|bibcode=2017CBio...27.1068B }}</ref> and modulates the transport of [[cytoskeletal]] structures and [[organelles]] such as [[mitochondria]], along the axon.<ref>{{cite journal|vauthors=Stassart RM, Möbius W, Nave KA, Edgar JM|title=The Axon-Myelin Unit in Development and Degenerative Disease|journal=Frontiers in Neuroscience|volume=12|page=467|year=2018|pmid=30050403|pmc=6050401|doi=10.3389/fnins.2018.00467 |doi-access=free}}</ref> In 2012, evidence came to light to support a role for the myelinating cell in "feeding" the axon.<ref>{{cite journal|vauthors=Fünfschilling U, Supplie LM, Mahad D, Boretius S, Saab AS, Edgar J, Brinkmann BG, Kassmann CM, Tzvetanova ID, Möbius W, Diaz F, Meijer D, Suter U, Hamprecht B, Sereda MW, Moraes CT, Frahm J, Goebbels S, Nave KA|title=Glycolytic oligodendrocytes maintain myelin and long-term axonal integrity|journal=Nature|volume=485|issue=7399|pages=517–21|date=April 2012|pmid=22622581|pmc=3613737|doi=10.1038/nature11007|bibcode=2012Natur.485..517F }}</ref><ref>{{cite journal|vauthors=Lee Y, Morrison BM, Li Y, Lengacher S, Farah MH, Hoffman PN, Liu Y, Tsingalia A, Jin L, Zhang PW, Pellerin L, Magistretti PJ, Rothstein JD|title=Oligodendroglia metabolically support axons and contribute to neurodegeneration|journal=Nature|volume=487|issue=7408|pages=443–48|date=July 2012|pmid=22801498|pmc=3408792|doi=10.1038/nature11314|bibcode=2012Natur.487..443L }}</ref> In other words, the myelinating cell seems to act as a local "fueling station" for the axon, which uses a great deal of energy to restore the normal balance of ions between it and its environment,<!-- Removed "see above and" - too vague, also should not use refs as though they were syntactically nouns; to re-cite previously cited refs, just repeat the ref tag with a name --><ref>{{cite journal|vauthors=Engl E, Attwell D|title=Non-signalling energy use in the brain|journal=The Journal of Physiology|volume=593|issue=16|pages=3417–329|date=August 2015|pmid=25639777|pmc=4560575|doi=10.1113/jphysiol.2014.282517 }}</ref><ref>{{cite journal|vauthors=Attwell D, Laughlin SB|title=An energy budget for signaling in the grey matter of the brain|journal=Journal of Cerebral Blood Flow and Metabolism|volume=21|issue=10|pages=1133–45|date=October 2001|pmid=11598490|doi=10.1097/00004647-200110000-00001 |doi-access=free}}</ref> following the generation of action potentials.

When a peripheral nerve fiber is severed, the myelin sheath provides a track along which regrowth can occur. However, the myelin layer does not ensure a perfect regeneration of the nerve fiber. Some regenerated nerve fibers do not find the correct muscle fibers, and some damaged motor neurons of the [[peripheral nervous system]] die without regrowth. Damage to the myelin sheath and nerve fiber is often associated with increased functional insufficiency.

Unmyelinated fibers and myelinated axons of the mammalian central nervous system do not regenerate.<ref>{{Cite journal|last1=Huebner|first1=Eric A.|last2=Strittmatter|first2=Stephen M.|date=2009|title=Axon Regeneration in the Peripheral and Central Nervous Systems|journal=Results and Problems in Cell Differentiation|volume=48|pages=339–51|doi=10.1007/400_2009_19|issn=0080-1844|pmc=2846285|pmid=19582408|isbn=978-3-642-03018-5}}</ref>