:Myelin

Myelin was first described as white matter fibres in 1717 by Vesalius, and first named as myelin by Rudolf Virchow in 1854.{{cite journal|vauthors=Boullerne AI|title=The history of myelin|journal=Experimental Neurology|volume=283|issue=Pt B|pages=431–45|date=September 2016|pmid=27288241|pmc=5010938|doi=10.1016/j.expneurol.2016.06.005 }} Over a century later, following the development of electron microscopy, its glial cell origin, and its ultrastructure became apparent.

Image:Myelinated neuron.jpg of a cross-section of a myelinated PNS axon, generated at the Electron Microscopy Facility at Trinity College, Hartford, Connecticut]]

[[File:Myelin sheath (1).svg|thumb|upright|Diagram of a myelinated axon in cross-section{{ordered list

|Axon

|Nucleus of Schwann cell

|Schwann cell

|Myelin sheath

|Neurilemma}}]]

Myelin is found in all vertebrates except the jawless fish. Myelin in the central nervous system (CNS) differs slightly in composition and configuration from myelin in the peripheral nervous system (PNS), but both perform the same functions of insulation and nutritional support. Being rich in lipid, myelin appears white, hence its earlier name of white matter of the CNS. Both CNS white matter tracts such as the corpus callosum, and corticospinal tract, and PNS nerves such as the sciatic nerve, and the auditory nerve, which also appear white, comprise thousands to millions of axons, largely aligned in parallel. In the corpus callosum there are more than 200 million axons.{{cite journal |vauthors=Luders E, Thompson PM, Toga AW |title=The development of the corpus callosum in the healthy human brain |journal=J Neurosci |volume=30 |issue=33 |pages=10985–90 |date=August 2010 |pmid=20720105 |pmc=3197828 |doi=10.1523/JNEUROSCI.5122-09.2010 |url=}} Blood vessels provide the route for oxygen and energy substrates such as glucose to reach these fibre tracts, which also contain other cell types including astrocytes and microglia in the CNS and macrophages in the PNS.

In terms of total mass, myelin comprises approximately 40% water; the dry mass comprises between 60% and 75% lipid and between 15% and 25% protein. Protein content includes myelin basic protein (MBP),{{cite journal|vauthors=Steinman L|title=Multiple sclerosis: a coordinated immunological attack against myelin in the central nervous system|journal=Cell|volume=85|issue=3|pages=299–302|date=May 1996|pmid=8616884|doi=10.1016/S0092-8674(00)81107-1 |s2cid=18442078|doi-access=free}} which is abundant in the CNS where it plays a critical, non-redundant role in formation of compact myelin; myelin oligodendrocyte glycoprotein (MOG),{{cite journal|vauthors=Mallucci G, Peruzzotti-Jametti L, Bernstock JD, Pluchino S|title=The role of immune cells, glia and neurons in white and gray matter pathology in multiple sclerosis|journal=Progress in Neurobiology|volume=127–128|pages=1–22|date=April 2015|pmid=25802011|pmc=4578232|doi=10.1016/j.pneurobio.2015.02.003 }} which is specific to the CNS; and proteolipid protein (PLP),{{cite journal|vauthors=Greer JM, Lees MB|title=Myelin proteolipid protein – the first 50 years|journal=The International Journal of Biochemistry & Cell Biology|volume=34|issue=3|pages=211–15|date=March 2002|pmid=11849988|doi=10.1016/S1357-2725(01)00136-4 }} which is the most abundant protein in CNS myelin, but only a minor component of PNS myelin. In the PNS, myelin protein zero (MPZ or P0) has a similar role to that of PLP in the CNS in that it is involved in holding together the multiple concentric layers of glial cell membrane that constitute the myelin sheath. The primary lipid of myelin is a glycolipid called galactocerebroside. The intertwining hydrocarbon chains of sphingomyelin strengthen the myelin sheath. Cholesterol is an essential lipid component of myelin, without which myelin fails to form.{{cite journal|vauthors=Saher G, Brügger B, Lappe-Siefke C, Möbius W, Tozawa R, Wehr MC, Wieland F, Ishibashi S, Nave KA|title=High cholesterol level is essential for myelin membrane growth|journal=Nature Neuroscience|volume=8|issue=4|pages=468–75|date=April 2005|pmid=15793579|doi=10.1038/nn1426 |s2cid=9762771}}

Myelin-associated glycoprotein (MAG) is a critical protein in the formation and maintenance of myelin sheaths. MAG is localized on the inner membrane of the myelin sheath and interacts with axonal membrane proteins to attach the myelin sheath to the axon.{{cite book | vauthors = Lopez PH | chapter = Role of Myelin-Associated Glycoprotein (Siglec-4a) in the Nervous System | series = Advances in Neurobiology | title = Glycobiology of the Nervous System | year = 2014 | volume = 9 | pages = 245–62 | pmid = 25151382 | doi = 10.1007/978-1-4939-1154-7_11 | isbn = 978-1-4939-1153-0 }} Mutations to the MAG gene are implicated in demyelination diseases such as multiple sclerosis.{{cite journal | vauthors = Pronker MF, Lemstra S, Snijder J, Heck AJ, Thies-Weesie DM, Pasterkamp RJ, Janssen BJ | title = Structural basis of myelin-associated glycoprotein adhesion and signalling | journal = Nature Communications | volume = 7 | pages = 13584 | date = December 2016 | pmid = 27922006 | doi = 10.1038/ncomms13584 | pmc = 5150538 | bibcode = 2016NatCo...713584P }}

{{Main|Saltatory conduction}}

File:Saltatory Conduction.gif.]]

The main purpose of myelin is to increase the speed at which electrical impulses (known as action potentials) 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.{{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}}

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.{{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}} Positively charged sodium ions 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.{{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/ }} The action potential "recharges" at consecutive nodes of Ranvier as the axolemmal membrane potential depolarises to approximately +35 mV. 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;{{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 }} and modulates the transport of cytoskeletal structures and organelles such as mitochondria, along the axon.{{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}} In 2012, evidence came to light to support a role for the myelinating cell in "feeding" the axon.{{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 }}{{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 }} 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,{{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 }}{{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}} 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.{{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}}

{{Main|Myelination}}

{{Further|Critical period#Myelin}}

The process of generating myelin is called myelination or myelinogenesis. In the CNS, oligodendrocyte progenitor cells differentiate into mature oligodendrocytes, which form myelin. In humans, myelination begins early in the third trimester which starts at around week 26 of gestational age.{{Cite web|url=http://library.med.utah.edu/pedineurologicexam/html/dev_anatomy.html|title=Pediatric Neurologic Examination Videos & Descriptions: Developmental Anatomy|website=library.med.utah.edu|access-date=2016-08-20}} The signal for myelination comes from the axon; axons larger than 1-2 μms become myelinated.{{cite book |last1=Schoenwolf |first1=Gary C. |last2=Bleyl |first2=Steven B. |last3=Brauer |first3=Philip R. |last4=Francis-West |first4=P. H. |title=Larsen's human embryology |date=2015 |publisher=Churchill Livingstone |location=Philadelphia, PA |isbn=9781455706846 |page=242 |edition=Fifth}} The length of the internode is determined by the size of the axonal diameter. During infancy, myelination progresses rapidly, with increasing numbers of axons acquiring myelin sheaths. This corresponds with the development of cognitive and motor skills, including language comprehension, speech acquisition, crawling and walking. Myelination continues through adolescence and early adulthood and although largely complete at this time, myelin sheaths can be added in grey matter regions such as the cerebral cortex, throughout life.{{cite journal|vauthors=Swire M, French-Constant C|title=Seeing Is Believing: Myelin Dynamics in the Adult CNS|journal=Neuron|volume=98|issue=4|pages=684–86|date=May 2018|pmid=29772200|doi=10.1016/j.neuron.2018.05.005 |doi-access=free}}{{cite journal|vauthors=Hill RA, Li AM, Grutzendler J|title=Lifelong cortical myelin plasticity and age-related degeneration in the live mammalian brain|journal=Nature Neuroscience|volume=21|issue=5|pages=683–95|date=May 2018|pmid=29556031|pmc=5920745|doi=10.1038/s41593-018-0120-6 }}{{cite journal|vauthors=Hughes EG, Orthmann-Murphy JL, Langseth AJ, Bergles DE|title=Myelin remodeling through experience-dependent oligodendrogenesis in the adult somatosensory cortex|journal=Nature Neuroscience|volume=21|issue=5|pages=696–706|date=May 2018|pmid=29556025|pmc=5920726|doi=10.1038/s41593-018-0121-5 }}

Not all axons are myelinated. For example, in the PNS, a large proportion of axons are unmyelinated. Instead, they are ensheathed by non-myelinating Schwann cells known as Remak SCs and arranged in Remak bundles.{{cite journal|vauthors=Monk KR, Feltri ML, Taveggia C|title=New insights on Schwann cell development|journal=Glia|volume=63|issue=8|pages=1376–93|date=August 2015|pmid=25921593|pmc=4470834|doi=10.1002/glia.22852 }} In the CNS, non-myelinated axons (or intermittently myelinated axons, meaning axons with long non-myelinated regions between myelinated segments) intermingle with myelinated ones and are entwined, at least partially, by the processes of another type of glial cell the astrocyte.{{Citation needed|date=July 2018}}{{Cite journal|last1=Wang|first1=Doris D.|last2=Bordey|first2=Angélique|date=11 December 2008|title=The astrocyte odyssey|journal=Progress in Neurobiology|volume=86|issue=4|pages=342–67|doi=10.1016/j.pneurobio.2008.09.015|pmid=18948166|via=Elsevier Science Direct|pmc=2613184}}

{{Further|Demyelinating disease|Lesional demyelinations of the central nervous system}}

Demyelination is the loss of the myelin sheath insulating the nerves, and is the hallmark of some neurodegenerative autoimmune diseases, including multiple sclerosis, acute disseminated encephalomyelitis, neuromyelitis optica, transverse myelitis, chronic inflammatory demyelinating polyneuropathy, Guillain–Barré syndrome, central pontine myelinosis, inherited demyelinating diseases such as leukodystrophy, and Charcot–Marie–Tooth disease. People with pernicious anaemia can also develop nerve damage if the condition is not diagnosed quickly. Subacute combined degeneration of spinal cord secondary to pernicious anaemia can lead to slight peripheral nerve damage to severe damage to the central nervous system, affecting speech, balance, and cognitive awareness. When myelin degrades, conduction of signals along the nerve can be impaired or lost, and the nerve eventually withers.{{Clarify|date=April 2014}} A more serious case of myelin deterioration is called Canavan disease.

The immune system may play a role in demyelination associated with such diseases, including inflammation causing demyelination by overproduction of cytokines via upregulation of tumor necrosis factor{{cite journal|vauthors=Ledeen RW, Chakraborty G|title=Cytokines, signal transduction, and inflammatory demyelination: review and hypothesis|journal=Neurochemical Research|volume=23|issue=3|pages=277–89|date=March 1998|pmid=9482240|doi=10.1023/A:1022493013904 |s2cid=7499162}} or interferon. MRI evidence that docosahexaenoic acid DHA ethyl ester improves myelination in generalized peroxisomal disorders.{{cite journal |last1=Martinez |first1=Manuela |last2=Vazquez |first2=Elida |title=MRI evidence that docosahexaenoic acid ethyl ester improves myelination in generalized peroxisomal disorders |journal=Neurology |date=1 July 1998 |volume=51 |issue=1 |pages=26–32 |doi=10.1212/wnl.51.1.26 |pmid=9674774 |s2cid=21929640 |url=https://n.neurology.org/content/51/1/26|url-access=subscription }}

Demyelination results in diverse symptoms determined by the functions of the affected neurons. It disrupts signals between the brain and other parts of the body; symptoms differ from patient to patient, and have different presentations upon clinical observation and in laboratory studies.

Typical symptoms include blurriness in the central visual field that affects only one eye, may be accompanied by pain upon eye movement, double vision, loss of vision/hearing, odd sensation in legs, arms, chest, or face, such as tingling or numbness (neuropathy), weakness of arms or legs, cognitive disruption, including speech impairment and memory loss, heat sensitivity (symptoms worsen or reappear upon exposure to heat, such as a hot shower), loss of dexterity, difficulty coordinating movement or balance disorder, difficulty controlling bowel movements or urination, fatigue, and tinnitus.Mayo Clinic 2007 and University of Leicester Clinical Studies, 2014{{full citation needed|date=July 2018}}

{{Further|Remyelination}}

Research to repair damaged myelin sheaths is ongoing. Techniques include surgically implanting oligodendrocyte precursor cells in the central nervous system and inducing myelin repair with certain antibodies. While results in mice have been encouraging (via stem cell transplantation), whether this technique can be effective in replacing myelin loss in humans is still unknown.{{cite journal|vauthors=Windrem MS, Nunes MC, Rashbaum WK, Schwartz TH, Goodman RA, McKhann G, Roy NS, Goldman SA|title=Fetal and adult human oligodendrocyte progenitor cell isolates myelinate the congenitally dysmyelinated brain|journal=Nature Medicine|volume=10|issue=1|pages=93–97|date=January 2004|pmid=14702638|doi=10.1038/nm974|s2cid=34822879}}

• {{cite web |date=January 20, 2004 |title=Stem Cell Therapy Replaces Missing Myelin In Mouse Brains |website=FuturePundit |url=http://www.futurepundit.com/archives/001901.html |access-date=March 22, 2007 |archive-date=June 14, 2011 |archive-url=https://web.archive.org/web/20110614173025/http://www.futurepundit.com/archives/001901.html |url-status=dead }} Cholinergic treatments, such as acetylcholinesterase inhibitors (AChEIs), may have beneficial effects on myelination, myelin repair, and myelin integrity. Increasing cholinergic stimulation also may act through subtle trophic effects on brain developmental processes and particularly on oligodendrocytes and the lifelong myelination process they support. Increasing oligodendrocyte cholinergic stimulation, AChEIs, and other cholinergic treatments, such as nicotine, possibly could promote myelination during development and myelin repair in older age.{{cite journal|vauthors=Bartzokis G|title=Acetylcholinesterase inhibitors may improve myelin integrity|journal=Biological Psychiatry|volume=62|issue=4|pages=294–301|date=August 2007|pmid=17070782|doi=10.1016/j.biopsych.2006.08.020 |s2cid=2130691}} Glycogen synthase kinase 3β inhibitors such as lithium chloride have been found to promote myelination in mice with damaged facial nerves.{{cite journal|vauthors=Makoukji J, Belle M, Meffre D, Stassart R, Grenier J, Shackleford G, Fledrich R, Fonte C, Branchu J, Goulard M, de Waele C, Charbonnier F, Sereda MW, Baulieu EE, Schumacher M, Bernard S, Massaad C|title=Lithium enhances remyelination of peripheral nerves|journal=Proceedings of the National Academy of Sciences of the United States of America|volume=109|issue=10|pages=3973–78|date=March 2012|pmid=22355115|pmc=3309729|doi=10.1073/pnas.1121367109|bibcode=2012PNAS..109.3973M |doi-access=free}} Cholesterol is a necessary nutrient for the myelin sheath, along with vitamin B12.{{cite journal|vauthors=Petrov AM, Kasimov MR, Zefirov AL|title=Brain Cholesterol Metabolism and Its Defects: Linkage to Neurodegenerative Diseases and Synaptic Dysfunction|journal=Acta Naturae|volume=8|issue=1|pages=58–73|date=2016|pmid=27099785|pmc=4837572 |doi=10.32607/20758251-2016-8-1-58-73}}{{cite journal|vauthors=Miller A, Korem M, Almog R, Galboiz Y|title=Vitamin B12, demyelination, remyelination and repair in multiple sclerosis|journal=Journal of the Neurological Sciences|volume=233|issue=1–2|pages=93–97|date=June 2005|pmid=15896807|doi=10.1016/j.jns.2005.03.009 |s2cid=6269094}}

Dysmyelination is characterized by a defective structure and function of myelin sheaths; unlike demyelination, it does not produce lesions. Such defective sheaths often arise from genetic mutations affecting the biosynthesis and formation of myelin. The shiverer mouse represents one animal model of dysmyelination. Human diseases where dysmyelination has been implicated include leukodystrophies (Pelizaeus–Merzbacher disease, Canavan disease, phenylketonuria) and schizophrenia.{{cite journal|vauthors=Krämer-Albers EM, Gehrig-Burger K, Thiele C, Trotter J, Nave KA|title=Perturbed interactions of mutant proteolipid protein/DM20 with cholesterol and lipid rafts in oligodendroglia: implications for dysmyelination in spastic paraplegia|journal=The Journal of Neuroscience|volume=26|issue=45|pages=11743–52|date=November 2006|pmid=17093095|pmc=6674790|doi=10.1523/JNEUROSCI.3581-06.2006 }}{{cite book|vauthors=Matalon R, Michals-Matalon K, Surendran S, Tyring SK|title=N-Acetylaspartate|chapter=Canavan disease: studies on the knockout mouse|series=Advances in Experimental Medicine and Biology|volume=576|pages=77–93; discussion 361–63|date=2006|pmid=16802706|doi=10.1007/0-387-30172-0_6|isbn=978-0-387-30171-6 }}{{cite journal|vauthors=Tkachev D, Mimmack ML, Huffaker SJ, Ryan M, Bahn S|title=Further evidence for altered myelin biosynthesis and glutamatergic dysfunction in schizophrenia|journal=The International Journal of Neuropsychopharmacology|volume=10|issue=4|pages=557–63|date=August 2007|pmid=17291371|doi=10.1017/S1461145706007334 |doi-access=free}}

Functionally equivalent myelin-like sheaths are found in several invertebrate taxa, including oligochaete annelids, and crustacean taxa such as penaeids, palaemonids, and calanoids. These myelin-like sheaths share several structural features with the sheaths found in vertebrates including multiplicity of membranes, condensation of membrane, and nodes. However, the nodes in vertebrates are annular; i.e. they encircle the axon. In contrast, nodes found in the sheaths of invertebrates are either annular or fenestrated; i.e. they are restricted to "spots". The fastest recorded conduction speed (across both vertebrates and invertebrates) is found in the ensheathed axons of the Kuruma shrimp, an invertebrate, ranging between 90 and 200 m/s{{cite journal|vauthors=Salzer JL, Zalc B|title=Myelination|journal=Current Biology|volume=26|issue=20|pages=R971–75|date=October 2016|pmid=27780071|doi=10.1016/j.cub.2016.07.074|url=http://hal.upmc.fr/hal-01390042/file/Salzer_2016_Myelination.pdf|doi-access=free|bibcode=2016CBio...26.R971S }} (cf. 100–120 m/s for the fastest myelinated vertebrate axon).

• Myelin-associated glycoprotein
• Myelin incisure
• The Myelin Project, project to regenerate myelin
• Myelin Repair Foundation, a nonprofit medical research foundation for multiple sclerosis drug discovery.
• Myelinoid, an in vitro model for studying human myelination and white matter diseases

{{Reflist}}

{{refbegin}}

• Fields, R. Douglas, "The Brain Learns in Unexpected Ways: Neuroscientists have discovered a set of unfamiliar cellular mechanisms for making fresh memories", Scientific American, vol. 322, no. 3 (March 2020), pp. 74–79. "Myelin, long considered inert insulation on axons, is now seen as making a contribution to learning by controlling the speed at which signals travel along neural wiring." (p. 79.)
• {{cite journal|vauthors=Swire M, Ffrench-Constant C|title=Seeing Is Believing: Myelin Dynamics in the Adult CNS|journal=Neuron|volume=98|issue=4|pages=684–86|date=May 2018|pmid=29772200|doi=10.1016/j.neuron.2018.05.005 |doi-access=free}}
• {{cite journal|vauthors=Waxman SG|title=Conduction in myelinated, unmyelinated, and demyelinated fibers|journal=Archives of Neurology|volume=34|issue=10|pages=585–89|date=October 1977|pmid=907529|doi=10.1001/archneur.1977.00500220019003 }}

{{refend}}

• [http://www.nationalmssociety.org/about-multiple-sclerosis/what-we-know-about-ms/what-is-ms/myelin/index.aspx The MS Information Sourcebook, Myelin]
• [https://web.archive.org/web/20061205015229/http://www-medlib.med.utah.edu/WebPath/HISTHTML/HISTOTCH/HISTOTCH.html H & E Histology]
• [https://web.archive.org/web/20080821112759/http://www-medlib.med.utah.edu/WebPath/HISTHTML/MANUALS/LFB.PDF Luxol Fast Blue: Modified Kluver's Method to stain for Myelin Sheath]

{{Nervous tissue}}

{{Structures of the cell membrane}}

{{Cell membrane proteins}}

Category:Neurohistology