Myelin - wikipedia Myelin Myelin Structure of simplified neuron in the PNS Neuron with oligodendrocyte and myelin sheath in the CNS Details System Nervous system Identifiers FMA 62977 Anatomical terminology ( edit on Wikidata ) Myelin is a lipid - rich ( fatty ) substance formed in the central nervous system ( CNS ) by glial cells called oligodendrocytes, and in the peripheral nervous system ( PNS ) by Schwann cells. Myelin insulates nerve cell axons to increase the speed at which information ( encoded as an electrical signal ) travels from one nerve cell body to another ( as in the CNS ) or, for example, from a nerve cell body to a muscle ( as in the PNS ). The myelinated axon can be likened to an electrical wire ( the axon ) with insulating material ( myelin ) around it. However, unlike the plastic covering on an electrical wire, myelin does not form a single long sheath over the entire length of the axon. Rather, each myelin sheath insulates the axon over a single section and, in general, each axon comprises multiple long myelinated sections separated from each other by short gaps. Each myelin sheath is formed by the concentric wrapping of an oligodendrocyte or Schwann cell process around the axon. More precisely, myelin speeds the transmission of electrical impulses called action potentials along myelinated axons by insulating the axon and reducing axonal membrane capacitance. This results in saltatory conduction whereby the action potential `` jumps '' from one node of Ranvier, over a long myelinated stretch of the axon called the internode, before ' recharging ' at the next node of Ranvier, and so on, until it reaches the axon terminal. Nodes of Ranvier are the short ( ~ 1 micron ) unmyelinated regions of the axon between adjacent long ( ~ 0.2 mm - > 1 mm ) myelinated internodes. Once it reaches the axon terminal, this electrical signal provokes the release of a chemical message or neurotransmitter that binds to receptors on the adjacent post-synaptic cell ( e.g. nerve cell in the CNS or muscle cell in the PNS ) at specialised regions called synapses. This `` insulating '' role for myelin is essential for normal motor function ( i.e. movement such as walking ), sensory function ( e.g. hearing, seeing or feeling the sensation of pain ) and cognition ( e.g. acquiring and recalling knowledge ), as demonstrated by the consequences of disorders that affect it, such as the genetically determined leukodystrophies ; the acquired inflammatory demyelinating disorder, multiple sclerosis ; and the inflammatory demyelinating peripheral neuropathies. Due to its high prevalence, multiple sclerosis, which specifically affects the central nervous system ( brain, spinal cord and optic nerve ), is the best known disorder of myelin. Contents 1 Development 2 Species distribution 3 Composition 4 Function 5 Clinical significance 5.1 Demyelination 5.1. 1 Symptoms 5.1. 2 Myelin repair 5.2 Dysmyelination 6 Invertebrate myelin 7 See also 8 References 9 Further reading 10 External links Development The process of generating myelin is called myelination or myelinogenesis. In the CNS, cells called oligodendrocyte precursor cells ( OPCs ; the precursors of oligodendrocytes ) synthesise myelin, and in so doing, transform into mature myelinating oligodendrocytes. In humans, myelination begins early in the 3rd trimester, although only little myelin is present in either the CNS or the PNS at the time of birth. 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. Species distribution Myelin is considered a defining characteristic of the jawed vertebrates ( gnathostomes ), but axons are ensheathed by glial cells in invertebrates, although these glial - wraps are quite different from vertebrate compact myelin, formed, as indicated above, by concentric wrapping of the myelinating cell process multiple times around the axon. Myelin was first described in 1854 by Rudolf Virchow, although it was over a century later, following the development of electron microscopy, that its glial cell origin and its ultrastructure became apparent.. In vertebrates, 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. In the CNS, non-myelinated ( or intermittently myelinated axons ; meaning having 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 called the astrocyte. Composition Transmission electron micrograph of a cross-section of a myelinated axon, generated at the Electron Microscopy Facility at Trinity College, Hartford CT Diagram of a myelinated axon in cross-section 1. Axon 2. Nucleus of Schwann cell 3. Schwann cell 4. Myelin sheath 5. Neurilemma CNS myelin differs slightly in composition and configuration from PNS myelin, but both perform the same `` insulating '' function ( see above ). Being rich in lipid, myelin appears white ; hence, the name given to the `` white matter '' of the CNS. Both CNS white matter tracts ( e.g. the optic nerve, corticospinal tract and corpus callosum ) and PNS nerves ( e.g. the sciatic nerve and the auditory nerve ; which also appear white ) each comprise thousands to millions of axons, largely aligned in parallel. 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 ), which is abundant in the CNS where it plays a critical, non-redundant role in formation of compact myelin ; myelin oligodendrocyte glycoprotein ( MOG ), which is specific to the CNS ; and proteolipid protein ( PLP, ) 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. Function 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 propagate along the myelinated fiber. In unmyelinated fibers, electrical impulses ( 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. 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. 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. 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 ( outwith 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 ; and modulates the transport of cytoskeletal structures and organelles such as mitochondria, along the axon. Recently, evidence came to light to support a role for the myelinating cell in `` feeding '' the axon. 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 ( see above and ), following the generation of action potentials. When a peripheral 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. Some studies have revealed that optic nerve fibers can be regenerated in postnatal rats. This regeneration depends upon two conditions : axonal die - back has to be prevented with appropriate neurotrophic factors, and neurite growth inhibitory components have to be inactivated. These studies may lead to further understanding of nerve fiber regeneration in the central nervous system. Clinical significance Demyelination Further information : Demyelinating disease 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. Sufferers of pernicious anaemia can also suffer 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. 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 or interferon. Symptoms 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 tinnitus Myelin repair Further information : 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. 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. By increasing oligodendrocyte cholinergic stimulation, AChEIs, and other cholinergic treatments, such as nicotine, possibly could promote myelination during development and myelin repair in older age. Glycogen synthase kinase 3β inhibitors such as lithium chloride have been found to promote myelination in mice with damaged facial nerves. Cholesterol is a necessary nutrient for the myelin sheath, along with vitamin B12. Dysmyelination 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. Invertebrate myelin Functionally equivalent myelin - like sheaths are found in several invertebrate taxa including Oligochaete, Penaeid, Palaemonid, 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. '' It is notable that 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 ( cf 100 - 120 m / s for the fastest myelinated vertebrate axon. ) See also Lesional demyelinations of the central nervous system The Myelin Project, project to regenerate myelin Myelin Repair Foundation, a nonprofit medical research foundation for multiple sclerosis drug discovery. References Jump up ^ Stassart RM, Möbius W, Nave KA, Edgar JM ( 2018 ). `` The Axon - Myelin Unit in Development and Degenerative Disease ''. Frontiers in Neuroscience. 12 : 467. doi : 10.3389 / fnins. 2018.00467. PMID 30050403. 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Jump up ^ Miller A, Korem M, Almog R, Galboiz Y ( June 2005 ). `` Vitamin B12, demyelination, remyelination and repair in multiple sclerosis ''. Journal of the Neurological Sciences. 233 ( 1 - 2 ) : 93 -- 7. doi : 10.1016 / j. jns. 2005.03. 009. PMID 15896807. Jump up ^ Krämer - Albers EM, Gehrig - Burger K, Thiele C, Trotter J, Nave KA ( November 2006 ). `` Perturbed interactions of mutant proteolipid protein / DM20 with cholesterol and lipid rafts in oligodendroglia : implications for dysmyelination in spastic paraplegia ''. The Journal of Neuroscience. 26 ( 45 ) : 11743 -- 52. doi : 10.1523 / JNEUROSCI. 3581 - 06.2006. PMID 17093095. Jump up ^ Matalon R, Michals - Matalon K, Surendran S, Tyring SK ( 2006 ). `` Canavan disease : studies on the knockout mouse ''. Advances in Experimental Medicine and Biology. 576 : 77 -- 93 ; discussion 361 -- 3. doi : 10.1007 / 0 - 387 - 30172 - 0_6. PMID 16802706. 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External links The Myelin Project Athabasca University Biological Psychology Website The MS Information Sourcebook, Myelin The Myelin Repair Foundation H & E Histology Luxol Fast Blue : Modified Kluver 's Method to stain for Myelin Sheath Radiology and Pathology of Myelin the MedPix Medical Image Database American Society for Neurochemistry Nervous tissue CNS Tissue Types Grey matter White matter Projection fibers Association fiber Commissural fiber Lemniscus Nerve tract Decussation Commissure Neuropil Meninges Cell Types Neuronal Pyramidal Purkinje Granule Glial insulating : Myelination : Oligodendrocyte other Astrocyte Radial glial cell Ependymal cells Tanycyte Microglia PNS General Dorsal Root Ganglion Ramus Ventral Root Ramus Ramus communicans Gray White Autonomic ganglion ( Preganglionic nerve fibers Postganglionic nerve fibers ) Nerve fascicle Funiculus Connective tissues Epineurium Perineurium Endoneurium Neuroglia Myelination : Schwann cell Neurilemma Myelin incisure Node of Ranvier Internodal segment Satellite glial cell Neurons / nerve fibers Parts Soma Axon hillock Axon Telodendron Axon terminals Axoplasm Axolemma Neurofibril / neurofilament Dendrite Nissl body Dendritic spine Apical dendrite / Basal dendrite Types Bipolar Unipolar Pseudounipolar Multipolar Interneuron Renshaw Afferent nerve fiber / Sensory neuron GSA GVA SSA SVA fibers Ia or Aα Ib or Golgi or Aα II or Aβ and Aγ III or Aδ or fast pain IV or C or slow pain Efferent nerve fiber / Motor neuron GSE GVE SVE Upper motor neuron Lower motor neuron α motorneuron β motorneuron γ motorneuron Termination Synapse Electrical synapse / Gap junction Chemical synapse Synaptic vesicle Active zone Postsynaptic density Autapse Ribbon synapse Neuromuscular junction Sensory receptors Meissner 's corpuscle Merkel nerve ending Pacinian corpuscle Ruffini ending Muscle spindle Free nerve ending Nociceptor Olfactory receptor neuron Photoreceptor cell Hair cell Taste bud Structures of the cell membrane Membrane lipids Lipid bilayer Phospholipids Lipoproteins Sphingolipids Sterols Membrane proteins Membrane glycoproteins Integral membrane proteins / transmembrane protein Peripheral membrane protein / Lipid - anchored protein Other Caveolae / Coated pits Cell junctions Glycocalyx Lipid raft / microdomains Membrane contact sites Membrane nanotubes Myelin sheath Nodes of Ranvier Nuclear envelope Phycobilisomes Porosomes Protein : cell membrane proteins ( other than Cell surface receptor, enzymes, and cytoskeleton ) Arrestin SAG ARRB1 ARRB2 ARR3 Membrane - spanning 4A MS4A1 MS4A2 MS4A3 MS4A4A MS4A4E MS4A5 MS4A6A MS4A6E MS4A7 MS4A8B MS4A9 MS4A10 MS4A12 MS4A13 MS4A14 MS4A15 MS4A18 Myelin Myelin basic protein PMP2 Myelin proteolipid protein PLP1 Myelin oligodendrocyte glycoprotein Myelin - associated glycoprotein Myelin protein zero Pulmonary surfactant Pulmonary surfactant - associated protein B Pulmonary surfactant - associated protein C Tetraspanin TSPAN1 TSPAN2 TSPAN3 TSPAN4 TSPAN5 TSPAN6 TSPAN7 TSPAN8 TSPAN9 TSPAN10 TSPAN11 TSPAN12 TSPAN13 TSPAN14 TSPAN15 TSPAN16 TSPAN17 TSPAN18 TSPAN19 TSPAN20 TSPAN21 TSPAN22 TSPAN23 TSPAN24 TSPAN25 TSPAN26 TSPAN27 TSPAN28 TSPAN29 TSPAN30 TSPAN31 TSPAN32 TSPAN33 TSPAN34 Other / ungrouped Calnexin LDL - receptor - related protein - associated protein Neurofibromin 2 Presenilin PSEN1 PSEN2 HFE Phospholipid transfer proteins Dysferlin STRC OTOF see also other cell membrane protein disorders Retrieved from `` https://en.wikipedia.org/w/index.php?title=Myelin&oldid=857137138 '' Categories : Neurohistology Hidden categories : Pages with unresolved properties Wikipedia articles needing page number citations from July 2018 Articles needing more detailed references All articles with unsourced statements Articles with unsourced statements from July 2018 Articles with unsourced statements from May 2011 Wikipedia articles needing clarification from April 2014 Talk Contents About Wikipedia Afrikaans Български Bosanski Català Čeština Dansk Deutsch Eesti Ελληνικά Español Euskara فارسی Français Gaeilge Galego 한국어 Հայերեն Ido Bahasa Indonesia Íslenska Italiano עברית Қазақша Magyar മലയാളം Nederlands 日本 語 Norsk Norsk nynorsk Occitan Polski Português Română Русский Simple English Slovenčina Slovenščina کوردی Suomi Svenska ไทย Türkçe Українська Tiếng Việt 中文 37 more Edit links This page was last edited on 29 August 2018, at 20 : 08 ( UTC ). 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Question: the myelin sheath that covers many cns axons is formed by
Answer: the concentric wrapping of an oligodendrocyte or Schwann cell process around the axon