Axon: Difference between revisions

An '''axon''' (from Greek ἄξων ''áxōn'', axis) or '''nerve fiber''' (or '''nerve''' '''fibre''': see [[American and British English spelling differences#-re, -er|spelling differences]]) is a long, slender [[cellular extensions|projection]] of a nerve cell, or [[neuron]], in [[Vertebrate|vertebrates]], that typically conducts electrical impulses known as [[action potential]]s away from the [[Soma (biology)|nerve cell body]]. The function of the axon is to transmit information to different neurons, muscles, and glands. In certain [[sensory neuron]]s ([[pseudounipolar neuron]]s), such as those for touch and warmth, the axons are called [[afferent nerve fiber]]s and the electrical impulse travels along these from the [[peripheral nervous system|periphery]] to the cell body and from the cell body to the spinal cord along another branch of the same axon. Axon dysfunction can be the cause of many inherited and acquired [[neurological disorder]]s that affect both the [[Peripheral nervous system|peripheral]] and [[Central nervous system|central neurons]]. Nerve fibers are [[Axon#Classification|classed]] into three types{{Snd}}[[group A nerve fiber]]s, [[group B nerve fiber]]s, and [[group C nerve fiber]]s. Groups A and B are [[myelin]]ated, and group C are unmyelinated. These groups include both sensory fibers and motor fibers. Another classification groups only the sensory fibers as Type I, Type II, Type III, and Type IV.

An axon is one of two types of [[Cellular extensions|cytoplasmic protrusions]] from the cell body of a neuron; the other type is a [[dendrite]]. Axons are distinguished from dendrites by several features, including shape (dendrites often taper while axons usually maintain a constant radius), length (dendrites are restricted to a small region around the cell body while axons can be much longer), and function (dendrites receive signals whereas axons transmit them). Some types of neurons have no axon and transmit signals from their dendrites. In some species, axons can emanate from dendrites known as axon-carrying dendrites.<ref name="Triarhou">{{cite journal | vauthors = Triarhou LC | title = Axons emanating from dendrites: phylogenetic repercussions with Cajalian hues | journal = Frontiers in Neuroanatomy | volume = 8 | pages = 133 | date = 2014 | pmid = 25477788 | pmc = 4235383 | doi = 10.3389/fnana.2014.00133 | doi-access = free }}</ref> No neuron ever has more than one axon; however in invertebrates such as insects or leeches the axon sometimes consists of several regions that function more or less independently of each other.<ref>{{cite journal | vauthors = Yau KW | title = Receptive fields, geometry and conduction block of sensory neurones in the central nervous system of the leech | journal = The Journal of Physiology | volume = 263 | issue = 3 | pages = 513–38 | date = December 1976 | pmid = 1018277 | pmc = 1307715 | doi = 10.1113/jphysiol.1976.sp011643 }}</ref>

Axons are covered by a membrane known as an [[axolemma]]; the cytoplasm within an axon is called [[axoplasm]]. Most axons branch, in some cases very profusely. The end branches of an axon are called [[telodendria]]. The swollen end of a telodendron is known as the [[axon terminal]] or end-foot which joins the dendrite or cell body of another neuron forming a [[Synapse|synaptic]] connection. Axons usually make contact with other neurons at junctions called [[synapse]]s but can also make contact with muscle or gland cells. In some circumstances, the axon of one neuron may form a synapse with the dendrites of the same neuron, resulting in an [[autapse]]. At a synapse, the [[Cell membrane|membrane]] of the axon closely adjoins the membrane of the target cell, and special molecular structures serve to transmit electrical or electrochemical signals across the gap. Some synaptic junctions appear along the length of an axon as it extends; these are called ''en passant boutons'' ("in passing boutons") and can be in the hundreds or even the thousands along one axon.<ref name="LS">{{cite book|last1=Squire|first1=Larry|title=Fundamental neuroscience|date=2013|publisher=Elsevier/Academic Press|location=Amsterdam|isbn=978-0-12-385-870-2|pages=61–65|edition=4th}}</ref> Other synapses appear as terminals at the ends of axonal branches.

A single axon, with all its branches taken together, can target multiple parts of the brain and generate thousands of synaptic terminals. A bundle of axons make a [[nerve tract]] in the [[central nervous system]],<ref name="Luders">{{cite journal | vauthors = Luders E, Thompson PM, Toga AW | title = The development of the corpus callosum in the healthy human brain | journal = The Journal of Neuroscience | volume = 30 | issue = 33 | pages = 10985–90 | date = August 2010 | pmid = 20720105 | pmc = 3197828 | doi = 10.1523/JNEUROSCI.5122-09.2010 }}</ref> and a [[nerve fascicle|fascicle]] in the [[peripheral nervous system]]. In [[Placentalia|placental mammals]] the largest [[white matter]] tract in the brain is the [[corpus callosum]], formed of some 200 million axons in the [[human brain]].<ref name="Luders" />

The '''axonal initial segment''' (AIS) is a structurally and functionally separate microdomain of the axon.<ref name="Nelson">{{cite journal | vauthors = Nelson AD, Jenkins PM | title = Axonal Membranes and Their Domains: Assembly and Function of the Axon Initial Segment and Node of Ranvier | journal = Frontiers in Cellular Neuroscience | volume = 11 | pages = 136 | date = 2017 | pmid = 28536506 | pmc = 5422562 | doi = 10.3389/fncel.2017.00136 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Leterrier C, Clerc N, Rueda-Boroni F, Montersino A, Dargent B, Castets F | title = Ankyrin G Membrane Partners Drive the Establishment and Maintenance of the Axon Initial Segment | language = en | journal = Frontiers in Cellular Neuroscience | volume = 11 | pages = 6 | date = 2017 | pmid = 28184187 | pmc = 5266712 | doi = 10.3389/fncel.2017.00006 | doi-access = free }}</ref> One function of the initial segment is to separate the main part of an axon from the rest of the neuron; another function is to help initiate action potentials.<ref>{{cite journal | vauthors = Leterrier C | title = The Axon Initial Segment: An Updated Viewpoint | journal = The Journal of Neuroscience | volume = 38 | issue = 9 | pages = 2135–2145 | date = February 2018 | pmid = 29378864 | pmc = 6596274 | doi = 10.1523/jneurosci.1922-17.2018 }}</ref> Both of these functions support neuron [[cell polarity]], in which dendrites (and, in some cases the [[Soma (biology)|soma]]) of a neuron receive input signals at the basal region, and at the apical region the neuron's axon provides output signals.<ref>{{cite journal | vauthors = Rasband MN | title = The axon initial segment and the maintenance of neuronal polarity | language = En | journal = Nature Reviews. Neuroscience | volume = 11 | issue = 8 | pages = 552–62 | date = August 2010 | pmid = 20631711 | doi = 10.1038/nrn2852 | s2cid = 23996233 }}</ref>

The axon initial segment is unmyelinated and contains a specialized complex of proteins. It is between approximately 20 and 60&nbsp;μm in length and functions as the site of action potential initiation.<ref name="Jones">{{cite journal | vauthors = Jones SL, Svitkina TM | title = Axon Initial Segment Cytoskeleton: Architecture, Development, and Role in Neuron Polarity | journal = Neural Plasticity | volume = 2016 | pages = 6808293 | date = 2016 | pmid = 27493806 | pmc = 4967436 | doi = 10.1155/2016/6808293 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Clark BD, Goldberg EM, Rudy B | title = Electrogenic tuning of the axon initial segment | journal = The Neuroscientist | volume = 15 | issue = 6 | pages = 651–68 | date = December 2009 | pmid = 20007821 | pmc = 2951114 | doi = 10.1177/1073858409341973 }}</ref> Both the position on the axon and the length of the AIS can change showing a degree of plasticity that can fine-tune the neuronal output.<ref name="Jones"/><ref name="Yamada">{{cite journal | vauthors = Yamada R, Kuba H | title = Structural and Functional Plasticity at the Axon Initial Segment | journal = Frontiers in Cellular Neuroscience | volume = 10 | pages = 250 | date = 2016 | pmid = 27826229 | pmc = 5078684 | doi = 10.3389/fncel.2016.00250 | doi-access = free }}</ref> A longer AIS is associated with a greater excitability.<ref name="Yamada"/> Plasticity is also seen in the ability of the AIS to change its distribution and to maintain the activity of neural circuitry at a constant level.<ref name="Susuki"/>

In other cases as seen in rat studies an axon originates from a dendrite; such axons are said to have "dendritic origin". Some axons with dendritic origin similarly have a "proximal" initial segment that starts directly at the axon origin, while others have a "distal" initial segment, discernibly separated from the axon origin.<ref name="Höfflin-2017" /> In many species some of the neurons have axons that emanate from the dendrite and not from the cell body, and these are known as axon-carrying dendrites.<ref name=Triarhou/> In many cases, an axon originates at an axon hillock on the soma; such axons are said to have "somatic origin". Some axons with somatic origin have a "proximal" initial segment adjacent the axon hillock, while others have a "distal" initial segment, separated from the soma by an extended axon hillock.<ref name="Höfflin-2017">{{cite journal | vauthors = Höfflin F, Jack A, Riedel C, Mack-Bucher J, Roos J, Corcelli C, Schultz C, Wahle P, Engelhardt M | display-authors = 6 | title = Heterogeneity of the Axon Initial Segment in Interneurons and Pyramidal Cells of Rodent Visual Cortex | language = en | journal = Frontiers in Cellular Neuroscience | volume = 11 | pages = 332 | date = 2017 | pmid = 29170630 | pmc = 5684645 | doi = 10.3389/fncel.2017.00332 | doi-access = free }}</ref>

In the normally developed brain, along the shaft of some axons are located pre-synaptic boutons also known as '''axonal varicosities''' and these have been found in regions of the [[hippocampus]] that function in the release of neurotransmitters.<ref name="Gu">{{cite journal |vauthors=Gu C |title=Rapid and Reversible Development of Axonal Varicosities: A New Form of Neural Plasticity |journal=Front Mol Neurosci |volume=14 |issue= |pages=610857 |date=2021 |pmid=33613192 |pmc=7886671 |doi=10.3389/fnmol.2021.610857 |url= |doi-access=free }}</ref> However, axonal varicosities are also present in neurodegenerative diseases where they interfere with the conduction of an action potential. Axonal varicosities are also the hallmark of [[traumatic brain injuries]].<ref name="Gu"/><ref name="Weber">{{cite journal |vauthors=Weber MT, Arena JD, Xiao R, Wolf JA, Johnson VE |title=CLARITY reveals a more protracted temporal course of axon swelling and disconnection than previously described following traumatic brain injury |journal=Brain Pathol |volume=29 |issue=3 |pages=437–450 |date=May 2019 |pmid=30444552 |pmc=6482960 |doi=10.1111/bpa.12677 |url=}}</ref> Axonal damage is usually to the axon cytoskeleton disrupting transport. As a consequence protein accumulations such as [[amyloid-beta precursor protein]] can build up in a swelling resulting in a number of varicosities along the axon.<ref name="Gu"/><ref name="Weber"/>

Extracellular recordings of action potential propagation in axons has been demonstrated in freely moving animals. While extracellular somatic action potentials have been used to study cellular activity in freely moving animals such as [[place cells]], axonal activity in both [[White matter|white]] and [[gray matter]] can also be recorded. Extracellular recordings of axon action potential propagation is distinct from somatic action potentials in three ways: 1. The signal has a shorter peak-trough duration (~150μs) than of [[pyramidal cell]]s (~500μs) or [[interneuron]]s (~250μs). 2. The voltage change is triphasic. 3. Activity recorded on a tetrode is seen on only one of the four recording wires. In recordings from freely moving rats, axonal signals have been isolated in white matter tracts including the alveus and the corpus callosum as well hippocampal gray matter.<ref>{{cite journal | vauthors = Robbins AA, Fox SE, Holmes GL, Scott RC, Barry JM | title = Short duration waveforms recorded extracellularly from freely moving rats are representative of axonal activity | journal = Frontiers in Neural Circuits | volume = 7 | issue = 181 | pages = 181 | date = Nov 2013 | pmid = 24348338 | pmc = 3831546 | doi = 10.3389/fncir.2013.00181 | doi-access = free }}</ref>

In addition to propagating action potentials to axonal terminals, the axon is able to amplify the action potentials, which makes sure a secure propagation of sequential action potentials toward the axonal terminal. In terms of molecular mechanisms, [[voltage-gated sodium channel]]s in the axons possess lower [[Threshold potential|threshold]] and shorter [[Refractory period (physiology)|refractory period]] in response to short-term pulses.<ref>{{cite journal | vauthors = Chen N, Yu J, Qian H, Ge R, Wang JH | title = Axons amplify somatic incomplete spikes into uniform amplitudes in mouse cortical pyramidal neurons | journal = PLOS ONE | volume = 5 | issue = 7 | pages = e11868 | date = July 2010 | pmid = 20686619 | pmc = 2912328 | doi = 10.1371/journal.pone.0011868 | bibcode = 2010PLoSO...511868C | doi-access = free }}</ref>

[[Netrin]] (also known as UNC-6) a secreted protein, functions in axon formation. When the [[UNC-5]] netrin receptor is mutated, several neurites are irregularly projected out of neurons and finally a single axon is extended anteriorly.<ref name="A">[[Neuroglia]] and [[pioneer neuron]]s express UNC-6 to provide global and local netrin cues for guiding migrations in [[Caenorhabditis elegans|''C. elegans'']]</ref><ref>{{cite journal | vauthors = Serafini T, Kennedy TE, Galko MJ, Mirzayan C, Jessell TM, Tessier-Lavigne M | title = The netrins define a family of axon outgrowth-promoting proteins homologous to C. elegans UNC-6 | journal = Cell | volume = 78 | issue = 3 | pages = 409–24 | date = August 1994 | pmid = 8062384 | doi = 10.1016/0092-8674(94)90420-0 | s2cid = 22666205 }}</ref><ref>{{cite journal | vauthors = Hong K, Hinck L, Nishiyama M, Poo MM, Tessier-Lavigne M, Stein E | title = A ligand-gated association between cytoplasmic domains of UNC5 and DCC family receptors converts netrin-induced growth cone attraction to repulsion | journal = Cell | volume = 97 | issue = 7 | pages = 927–41 | date = June 1999 | pmid = 10399920 | doi = 10.1016/S0092-8674(00)80804-1 | s2cid = 18043414 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Hedgecock EM, Culotti JG, Hall DH | title = The unc-5, unc-6, and unc-40 genes guide circumferential migrations of pioneer axons and mesodermal cells on the epidermis in C. elegans | journal = Neuron | volume = 4 | issue = 1 | pages = 61–85 | date = January 1990 | pmid = 2310575 | doi = 10.1016/0896-6273(90)90444-K | s2cid = 23974242 }}</ref> The neurotrophic factors{{Snd}}[[nerve growth factor]] (NGF), [[brain-derived neurotrophic factor]] (BDNF) and [[neurotrophin-3]] (NTF3) are also involved in axon development and bind to [[Trk receptor]]s.<ref>{{cite journal | vauthors = Huang EJ, Reichardt LF | s2cid = 10217268 | title = Trk receptors: roles in neuronal signal transduction | journal = Annual Review of Biochemistry | volume = 72 | pages = 609–42 | year = 2003 | pmid = 12676795 | doi = 10.1146/annurev.biochem.72.121801.161629 }}</ref>

Cells called [[guidepost cells]] assist in the [[axon guidance|guidance]] of neuronal axon growth. These cells that help [[axon guidance]], are typically other neurons that are sometimes immature. When the axon has completed its growth at its connection to the target, the diameter of the axon can increase by up to five times, depending on the [[Nerve conduction velocity|speed of conduction]] required.<ref name="Alberts">{{cite book |last1=Alberts |first1=Bruce |title=Molecular biology of the cell |date=2015 |isbn=9780815344643 |page=947 |edition=Sixth}}</ref>

It has also been discovered through research that if the axons of a neuron were damaged, as long as the soma (the cell body of a neuron) is not damaged, the axons would regenerate and remake the synaptic connections with neurons with the help of [[guidepost cells]]. This is also referred to as [[neuroregeneration]].<ref>{{cite journal | vauthors = Kunik D, Dion C, Ozaki T, Levin LA, Costantino S | title = Laser-based single-axon transection for high-content axon injury and regeneration studies | journal = PLOS ONE | volume = 6 | issue = 11 | pages = e26832 | year = 2011 | pmid = 22073205 | pmc = 3206876 | doi = 10.1371/journal.pone.0026832 | bibcode = 2011PLoSO...626832K | doi-access = free }}</ref>

Axons vary largely in length from a few micrometers up to meters in some animals. This emphasizes that there must be a cellular length regulation mechanism allowing the neurons both to sense the length of their axons and to control their growth accordingly. It was discovered that [[motor proteins]] play an important role in regulating the length of axons.<ref>{{cite journal | vauthors = Myers KA, Baas PW | title = Kinesin-5 regulates the growth of the axon by acting as a brake on its microtubule array | journal = The Journal of Cell Biology | volume = 178 | issue = 6 | pages = 1081–91 | date = September 2007 | pmid = 17846176 | pmc = 2064629 | doi = 10.1083/jcb.200702074 }}</ref> Based on this observation, researchers developed an explicit model for axonal growth describing how motor proteins could affect the axon length on the molecular level.<ref>{{cite journal | vauthors = Rishal I, Kam N, Perry RB, Shinder V, Fisher EM, Schiavo G, Fainzilber M | title = A motor-driven mechanism for cell-length sensing | journal = Cell Reports | volume = 1 | issue = 6 | pages = 608–16 | date = June 2012 | pmid = 22773964 | pmc = 3389498 | doi = 10.1016/j.celrep.2012.05.013 }}</ref><ref>{{cite journal | vauthors = Karamched BR, Bressloff PC | title = Delayed feedback model of axonal length sensing | journal = Biophysical Journal | volume = 108 | issue = 9 | pages = 2408–19 | date = May 2015 | pmid = 25954897 | pmc = 4423051 | doi = 10.1016/j.bpj.2015.03.055 | bibcode = 2015BpJ...108.2408K }}</ref><ref>{{cite journal | vauthors = Bressloff PC, Karamched BR | title = A frequency-dependent decoding mechanism for axonal length sensing | journal = Frontiers in Cellular Neuroscience | volume = 9 | pages = 281 | year = 2015 | pmid = 26257607 | pmc = 4508512 | doi = 10.3389/fncel.2015.00281 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Folz F, Wettmann L, [[Giovanna Morigi|Morigi G]], Kruse K | title = Sound of an axon's growth | journal = Physical Review E | volume = 99 | issue = 5–1 | pages = 050401 | date = May 2019 | pmid = 31212501 | doi = 10.1103/PhysRevE.99.050401 | arxiv = 1807.04799 | bibcode = 2019PhRvE..99e0401F | s2cid = 118682719 }}</ref> These studies suggest that motor proteins carry signaling molecules from the soma to the growth cone and vice versa whose concentration oscillates in time with a length-dependent frequency.

! Type !! Erlanger-Gasser<br />Classification || Diameter<br />(μm) || Myelin<ref>{{cite book |first1=Gillian |last1=Pocock | first2 = Christopher D | last2 = Richards | name-list-style = vanc |title=Human Physiology |location=New York |publisher=Oxford University Press |edition=2nd |year=2004 |pages=187–189 |isbn=978-0-19-858527-5 |display-authors=etal}}</ref> || Conduction<br />velocity (m/s)

| B || 1–5 || Yes || 3–15

| C || 0.2–1.5 || No || 0.5–2.0

a result of the axonal protein [[NMNAT2]], being prevented from reaching all of the axon.<ref name="Gilley">{{cite journal | vauthors = Gilley J, Coleman MP | title = Endogenous Nmnat2 is an essential survival factor for maintenance of healthy axons | journal = PLOS Biology | volume = 8 | issue = 1 | pages = e1000300 | date = January 2010 | pmid = 20126265 | pmc = 2811159 | doi = 10.1371/journal.pbio.1000300 | doi-access = free }}</ref>

A severe [[traumatic brain injury]] can result in widespread lesions to nerve tracts damaging the axons in a condition known as [[diffuse axonal injury]]. This can lead to a [[persistent vegetative state]].<ref name="Healthcare">{{cite web|url=http://www.medcyclopaedia.com/library/topics/volume_vi_1/b/BRAIN_INJURY_TRAUMATIC.aspx|archive-url=https://archive.today/20110526162429/http://www.medcyclopaedia.com/library/topics/volume_vi_1/b/BRAIN_INJURY_TRAUMATIC.aspx|url-status=dead|archive-date=26 May 2011|title=Brain Injury, Traumatic|publisher=[[General Electric|GE]]|website=Medcyclopaedia|access-date=20 June 2018}}</ref> It has been shown in studies on the [[rat]] that axonal damage from a single mild traumatic brain injury, can leave a susceptibility to further damage, after repeated mild traumatic brain injuries.<ref>{{cite journal | vauthors = Wright DK, Brady RD, Kamnaksh A, Trezise J, Sun M, McDonald SJ, Mychasiuk R, Kolbe SC, Law M, Johnston LA, O'Brien TJ, Agoston DV, Shultz SR | display-authors = 6 | title = Repeated mild traumatic brain injuries induce persistent changes in plasma protein and magnetic resonance imaging biomarkers in the rat | journal = Scientific Reports | volume = 9 | issue = 1 | pages = 14626 | date = October 2019 | pmid = 31602002 | pmc = 6787341 | doi = 10.1038/s41598-019-51267-w | bibcode = 2019NatSR...914626W }}</ref>

German anatomist [[Otto Friedrich Karl Deiters]] is generally credited with the discovery of the axon by distinguishing it from the dendrites.<ref name="Debanne" /> Swiss [[Albert von Kölliker|Rüdolf Albert von Kölliker]] and German [[Robert Remak]] were the first to identify and characterize the axon initial segment. Kölliker named the axon in 1896.<ref>{{cite book |title=Origins of neuroscience: a history of explorations into brain function| last=Finger |first=Stanley | name-list-style = vanc |publisher=Oxford University Press|year=1994|isbn=9780195146943|pages=47|oclc=27151391|quote=Kölliker would give the "axon" its name in 1896.}}</ref> [[Louis-Antoine Ranvier]] was the first to describe the gaps or nodes found on axons and for this contribution these axonal features are now commonly referred to as the [[Node of Ranvier|nodes of Ranvier]]. [[Santiago Ramón y Cajal]], a Spanish anatomist, proposed that axons were the output components of neurons, describing their functionality.<ref name="Debanne" /> [[Joseph Erlanger]] and [[Herbert Gasser]] earlier developed the classification system for peripheral nerve fibers,<ref>{{cite journal | vauthors = Grant G | title = The 1932 and 1944 Nobel Prizes in physiology or medicine: rewards for ground-breaking studies in neurophysiology | journal = Journal of the History of the Neurosciences | volume = 15 | issue = 4 | pages = 341–57 | date = December 2006 | pmid = 16997762 | doi = 10.1080/09647040600638981 | s2cid = 37676544 }}</ref> based on axonal conduction velocity, [[myelin]]ation, fiber size etc. [[Alan Hodgkin]] and [[Andrew Huxley]] also employed the squid giant axon (1939) and by 1952 they had obtained a full quantitative description of the ionic basis of the action potential, leading to the formulation of the [[Hodgkin–Huxley model]]. Hodgkin and Huxley were awarded jointly the [[Nobel Prize in Physiology or Medicine|Nobel Prize]] for this work in 1963. The formulae detailing axonal conductance were extended to vertebrates in the Frankenhaeuser–Huxley equations. The understanding of the biochemical basis for action potential propagation has advanced further, and includes many details about individual [[ion channel]]s.

The axons in [[invertebrate]]s have been extensively studied. The [[longfin inshore squid]], often used as a [[model organism]] has the longest known axon.<ref name="Hellier">{{Cite book|last1=Hellier|first1=Jennifer L.|title=The Brain, the Nervous System, and Their Diseases [3 volumes]|url=https://books.google.com/books?id=SDi2BQAAQBAJ&q=axon|publisher=ABC-CLIO|language=en|date=16 December 2014|url-status=live|archive-url=https://web.archive.org/web/20180314180028/https://books.google.co.uk/books?redir_esc=y&id=SDi2BQAAQBAJ&q=axon |archive-date=14 March 2018|isbn=9781610693387}}</ref> The [[giant squid]] has the largest axon known. Its size ranges from 0.5 (typically) to 1&nbsp;mm in diameter and is used in the control of its [[jet propulsion]] system. The fastest recorded conduction speed of 210&nbsp;m/s, is found in the ensheathed axons of some pelagic [[Penaeidae|Penaeid shrimp]]s<ref>{{cite journal | vauthors = Hsu K, Terakawa S | title = Fenestration in the myelin sheath of nerve fibers of the shrimp: a novel node of excitation for saltatory conduction | journal = Journal of Neurobiology | volume = 30 | issue = 3 | pages = 397–409 | date = July 1996 | pmid = 8807532 | doi = 10.1002/(SICI)1097-4695(199607)30:3<397::AID-NEU8>3.0.CO;2-# }}</ref> and the usual range is between 90 and 200&nbsp;meters/s<ref name=Salzer>{{cite journal | vauthors = Salzer JL, Zalc B | title = Myelination | journal = Current Biology | volume = 26 | issue = 20 | pages = R971–R975 | date = October 2016 | pmid = 27780071 | doi = 10.1016/j.cub.2016.07.074 | doi-access = free | bibcode = 2016CBio...26.R971S }}</ref> ([[Cf.|cf]] 100–120&nbsp;m/s for the fastest myelinated vertebrate axon.)