Myelin

Source: Wikipedia, the free encyclopedia.
Myelin formed by Schwann cells in the PNS
Myelin
Structure of simplified neuron in the PNS
Neuron with oligodendrocyte and myelin sheath in the CNS
Details
SystemNervous system
Identifiers
FMA62977
Anatomical terminology

Myelin (

axons (the nervous system's electrical wires) to insulate them and increase the rate at which electrical impulses (called action potentials) pass along the axon.[1][2] 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, myelin ensheaths the axon segmentally: in general, each axon is encased in multiple long sheaths with short gaps between, called nodes of Ranvier
. At the nodes of Ranvier, which are approximately one thousandth of a mm in length, the axon's membrane is bare of myelin.

Myelin's best known function is to increase the rate at which information, encoded as electrical charges, passes along the axon's length. Myelin achieves this by eliciting saltatory conduction,[3]. Saltatory conduction refers to the fact that electrical impulses 'jump' along the axon, over long myelin sheaths, from one node of Ranvier to the next. Thus, information is passed around 100 times faster along a myelinated axon than a non-myelinated one.

At the molecular level, the myelin sheath increases the distance between extracellular and intracellular ions, reducing the accumulation of electrical charges. The discontinuous structure of the myelin sheath results in the action potential "jumping" from one node of Ranvier over a long (c. 0.1 mm – >1 mm, or 100-1000 micron) myelinated stretch of the axon called the

secretory cell
).

Myelin is made by

neurolemmocytes (Schwann cells), which only myelinate a section of one axon. In the CNS, axons carry electrical signals from one nerve cell body to another.[7][8]
The "insulating" function for myelin is essential for efficient
peripheral neuropathies.[11]
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.

Development

Main article: Myelinogenesis
Further information: Critical period § Myelin

The process of generating myelin is called myelination or

oligodendrocyte progenitor cells (OPCs) differentiate into mature oligodendrocytes, which form myelin. In humans, myelination begins early in the 3rd trimester,[12] 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.[13][14][15]

Species distribution

Vertebrates

Myelin is considered a defining characteristic of the

gnathostomes), though axons are ensheathed by a type of cell, called glial cells, in invertebrates.[16][17] 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,[18] although it was over a century later, following the development of electron microscopy, that its glial cell origin and its ultrastructure became apparent.[19]

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

glial cell the astrocyte.[citation needed][21]

Invertebrates

Functionally equivalent myelin-like sheaths are found in several invertebrate taxa, including

calanoids. These myelin-like sheaths share several structural features with the sheaths found in vertebrates including multiplicity of membranes, condensation of membrane, and nodes.[16] 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,[16] ranging between 90 and 200 m/s[17] (cf.
100–120 m/s for the fastest myelinated vertebrate axon).

Composition

Transmission electron micrograph of a cross-section of a myelinated PNS axon, generated at the Electron Microscopy Facility at Trinity College, Hartford, Connecticut
Myelin sheath
  • 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 "

    macrophages
    in the PNS.

    In terms of total mass, myelin comprises approximately 40% water; the dry mass comprises between 60% and 75%

    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.[25]

    Function

    Main article: Saltatory conduction
    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

    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.[16]

    Myelinated fibers lack

    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.[27] The action potential "recharges" at consecutive nodes of Ranvier as the axolemmal membrane potential depolarises to approximately +35 mV.[26]
    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

    mitochondria, along the axon.[29] In 2012, evidence came to light to support a role for the myelinating cell in "feeding" the axon.[30][31] 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,[32][33]
    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.[34]

    Clinical significance

    Demyelination

    Further information: Demyelinating disease

    Demyelination is the loss of the myelin sheath insulating the nerves, and is the hallmark of some

    cognitive awareness. When myelin degrades, conduction of signals along the nerve can be impaired or lost, and the nerve eventually withers.[clarification needed] A more serious case of myelin deterioration is called Canavan disease
    .

    The

    tumor necrosis factor[35] or interferon. MRI evidence that docosahexaenoic acid DHA ethyl ester improves myelination in generalized peroxisomal disorders.[36]

    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, and tinnitus.[37]

    Myelin repair

    Further information: Remyelination

    Research to repair damaged myelin sheaths is ongoing. Techniques include surgically implanting

    Glycogen synthase kinase 3β inhibitors such as lithium chloride have been found to promote myelination in mice with damaged facial nerves.[40] Cholesterol is a necessary nutrient for the myelin sheath, along with vitamin B12.[41][42]

    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.[43][44][45]

    See also

    References

    1. S2CID 205503852
      .
    2. ^ Morell, Pierre; Quarles, Richard H. (1999). "The Myelin Sheath". Basic Neurochemistry: Molecular, Cellular and Medical Aspects. 6th edition. Lippincott-Raven. Retrieved 15 December 2023.
    3. S2CID 205503852
      .
    4. PMID 28340093
      .
    5. PMID 9675162
      .
    6. PMID 10339541
      .
    7. PMID 30050403
      .
    8. PMID 31066630
      .
    9. PMID 28638987
      .
    10. S2CID 195686659
      .
    11. S2CID 4961339
      .
    12. ^ "Pediatric Neurologic Examination Videos & Descriptions: Developmental Anatomy". library.med.utah.edu. Retrieved 2016-08-20.
    13. PMID 29772200
      .
    14. PMID 29556031
      .
    15. PMID 29556025
      .
    16. ^
      S2CID 33164806
      .
    17. ^
      PMID 27780071
      .
    18. S2CID 20120269
      .
    19. PMID 27288241
      .
    20. PMID 25921593
      .
    21. PMID 18948166
      – via Elsevier Science Direct.
    22. S2CID 18442078
      .
    23. PMID 25802011
      .
    24. PMID 11849988
      .
    25. S2CID 9762771
      .
    26. ^ a b Saladin KS (2012). Anatomy & physiology: the unity of form and function (6th ed.). New York, NY: McGraw-Hill.[page needed]
    27. ^ Raine CS (1999). "Characteristics of Neuroglia". In Siegel GJ, Agranoff BW, Albers RW, Fisher SK, Uhler MD (eds.). Basic Neurochemistry: Molecular, Cellular and Medical Aspects (6th ed.). Philadelphia: Lippincott-Raven.
    28. PMID 28318976
      .
    29. PMID 30050403
      .
    30. PMID 22622581
      .
    31. PMID 22801498
      .
    32. PMID 25639777
      .
    33. PMID 11598490
      .
    34. PMID 19582408
      .
    35. S2CID 7499162
      .
    36. S2CID 21929640
      .
    37. ^ Mayo Clinic 2007 and University of Leicester Clinical Studies, 2014[full citation needed]
    38. S2CID 34822879
      .
    39. S2CID 2130691
      .
    40. PMID 22355115
      .
    41. PMID 27099785
      .
    42. S2CID 6269094
      .
    43. PMID 17093095
      .
    44. PMID 16802706
      .
    45. PMID 17291371
      .

    Further reading

    External links
    Retrieved from "https://en.wikipedia.org/w/index.php?title=Myelin&oldid=1217046640"
    This page is based on the copyrighted Wikipedia article: Myelin. Articles is available under the CC BY-SA 3.0 license; additional terms may apply.Privacy Policy