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Axon
FromWikipedia,thefreeencyclopedia

Anaxon(fromGreekxn,
Structureofatypicalneuron
axis),isalong,slenderprojectionofa
nervecell,orneuron,thattypically
Axon
conductselectricalimpulsesaway
Axon
Dendrite
fromtheneuron'scellbody.
terminal
Myelinatedaxonsareknownasnerve
Nodeof
fibers.Thefunctionoftheaxonisto
Ranvier
Soma
transmitinformationtodifferent
neurons,musclesandglands.In
certainsensoryneurons
Axon
(pseudounipolarneurons),suchas
thosefortouchandwarmth,the
electricalimpulsetravelsalongan
Schwanncell
axonfromtheperipherytothecell
Myelinsheath
body,andfromthecellbodytothe
Nucleus
spinalcordalonganotherbranchof
thesameaxon.Axondysfunctioncausesmanyinheritedandacquiredneurologicaldisorderswhichcan
affectboththeperipheralandcentralneurons.
Anaxonisoneoftwotypesofprotoplasmicprotrusionsthatextrudefromthecellbodyofaneuron,the
othertypebeingdendrites.Axonsaredistinguishedfromdendritesbyseveralfeatures,includingshape
(dendritesoftentaperwhileaxonsusuallymaintainaconstantradius),length(dendritesarerestrictedto
asmallregionaroundthecellbodywhileaxonscanbemuchlonger),andfunction(dendritesusually
receivesignalswhileaxonsusuallytransmitthem).Alloftheseruleshaveexceptions,however.
Sometypesofneuronshavenoaxonandtransmitsignalsfromtheirdendrites.Noneuroneverhasmore
thanoneaxonhoweverininvertebratessuchasinsectsorleechestheaxonsometimesconsistsof
severalregionsthatfunctionmoreorlessindependentlyofeachother.[1]Mostaxonsbranch,insome
casesveryprofusely.
Axonsmakecontactwithothercellsusuallyotherneuronsbutsometimesmuscleorglandcellsat
junctionscalledsynapses.Atasynapse,themembraneoftheaxoncloselyadjoinsthemembraneofthe
targetcell,andspecialmolecularstructuresservetotransmitelectricalorelectrochemicalsignalsacross
thegap.Somesynapticjunctionsappearpartwayalonganaxonasitextendsthesearecalleden
passant("inpassing")synapses.Othersynapsesappearasterminalsattheendsofaxonalbranches.A
singleaxon,withallitsbranchestakentogether,caninnervatemultiplepartsofthebrainandgenerate
thousandsofsynapticterminals.

Contents
1 Anatomy
1.1 Initialsegment
1.2 NodesofRanvier
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2 Actionpotentials
3 Developmentandgrowth
3.1 Development
3.1.1 Extracellularsignaling
3.1.2 Intracellularsignaling
3.1.3 Cytoskeletaldynamics
3.2 Growth
4 History
5 Injury
6 Classification
6.1 Motor
6.2 Sensory
6.3 Autonomic
7 Seealso
8 References
9 Externallinks

Anatomy
Axonsaretheprimarytransmissionlinesofthenervoussystem,andasbundlestheyformnerves.Some
axonscanextenduptoonemeterormorewhileothersextendaslittleasonemillimeter.Thelongest
axonsinthehumanbodyarethoseofthesciaticnerve,whichrunfromthebaseofthespinalcordtothe
bigtoeofeachfoot.Thediameterofaxonsisalsovariable.Mostindividualaxonsaremicroscopicin
diameter(typicallyaboutonemicrometer(m)across).Thelargestmammalianaxonscanreacha
diameterofupto20m.Thesquidgiantaxon,whichisspecializedtoconductsignalsveryrapidly,is
closeto1millimetreindiameter,thesizeofasmallpencillead.Axonalarborization(thebranching
structureattheendofanervefiber)alsodiffersfromonenervefibertothenext.Axonsinthecentral
nervoussystemtypicallyshowcomplextreeswithmanybranchpoints.Incomparison,thecerebellar
granulecellaxonischaracterizedbyasingleTshapedbranchnodefromwhichtwoparallelfibers
extend.Elaboratearborizationallowsforthesimultaneoustransmissionofmessagestoalargenumber
oftargetneuronswithinasingleregionofthebrain.
Therearetwotypesofaxonsoccurringintheperipheralsystemandthecentralnervoussystem:
unmyelinatedandmyelinatedaxons.[2]Myelinisalayerofafattyinsulatingsubstance,whichisformed
bytwotypesofglialcells:Schwanncellsensheathingperipheralneuronsandoligodendrocytes
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insulatingthoseofthecentralnervoussystem.Alongmyelinatednerve
fibers,gapsinthemyelinsheathknownasnodesofRanvieroccurat
evenlyspacedintervals.Themyelinationenablesanespeciallyrapid
modeofelectricalimpulsepropagationcalledsaltatoryconduction.
Demyelinationofaxonscausesthemultitudeofneurologicalsymptoms
foundinthediseasemultiplesclerosis.
Ifthebrainofavertebrateis
extractedandslicedintothin
sections,somepartsofeach
sectionappeardarkandother
partslighterincolor.Thedark
partsareknownasgreymatter
andthelighterpartsaswhite
Crosssectionofanaxon.
matter.Whitemattergetsitslight
1.Axon
colorfromthemyelinsheathsof
Adissectedhumanbrain,showing
2.NucleusofSchwannCell
axons:thewhitematterpartsof
greymatterandwhitematter
3.SchwannCell
thebrainarecharacterizedbya
4.MyelinSheath
highdensityofmyelinatedaxons
5.Neurilemma
passingthroughthem,andalowdensityofcellbodiesofneurons.The
cerebralcortexhasathicklayerofgreymatteronthesurfaceandalarge
volumeofwhitematterunderneath:whatthismeansisthatmostofthesurfaceisfilledwithneuroncell
bodies,whereasmuchoftheareaunderneathisfilledwithmyelinatedaxonsthatconnecttheseneurons
toeachother.

Initialsegment
Theaxoninitialsegmentthethick,unmyelinatedpartofanaxonthatconnectsdirectlytothecell
bodyconsistsofaspecializedcomplexofproteins.Itisapproximately25minlengthandfunctions
asthesiteofactionpotentialinitiation.[3]Thedensityofvoltagegatedsodiumchannelsismuchhigher
intheinitialsegmentthanintheremainderoftheaxonorintheadjacentcellbody,exceptingtheaxon
hillock.[4]Thevoltagegatedionchannelsareknowntobefoundwithincertainareasoftheaxonal
membraneandinitiateactionpotential,conduction,andsynaptictransmission.[2]

NodesofRanvier
NodesofRanvier(alsoknownasmyelinsheathgaps)areshortunmyelinatedsegmentsofamyelinated
axon,whicharefoundperiodicallyinterspersedbetweensegmentsofthemyelinsheath.Therefore,at
thepointofthenodeofRanvier,theaxonisreducedindiameter.[5]Thesenodesareareaswhereaction
potentialscanbegenerated.Insaltatoryconduction,electricalcurrentsproducedateachnodeofRanvier
areconductedwithlittleattenuationtothenextnodeinline,wheretheyremainstrongenoughto
generateanotheractionpotential.Thusinamyelinatedaxon,actionpotentialseffectively"jump"from
nodetonode,bypassingthemyelinatedstretchesinbetween,resultinginapropagationspeedmuch
fasterthaneventhefastestunmyelinatedaxoncansustain.

Actionpotentials
Mostaxonscarrysignalsintheform
ofactionpotentials,whichare
discreteelectrochemicalimpulsesthat
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travelrapidlyalonganaxon,starting
Neurotransmitter
atthecellbodyandterminatingat
Neurotransmitter
pointswheretheaxonmakessynaptic
transporter
Synaptic
Axon
contactwithtargetcells.Thedefining
vesicle
characteristicofanactionpotentialis
terminal
thatitis"allornothing"every
Voltage
actionpotentialthatanaxon
gatedCa++
generateshasessentiallythesame
Synaptic
channel
sizeandshape.Thisallornothing
Receptor
cleft
Postsynaptic
characteristicallowsactionpotentials
density
Dendrite
tobetransmittedfromoneendofa
longaxontotheotherwithoutany
reductioninsize.Thereare,however,sometypesofneuronswithshortaxonsthatcarrygraded
electrochemicalsignals,ofvariableamplitude.
Whenanactionpotentialreachesapresynapticterminal,itactivatesthesynaptictransmissionprocess.
Thefirststepisrapidopeningofcalciumionchannelsinthemembraneoftheaxon,allowingcalcium
ionstoflowinwardacrossthemembrane.Theresultingincreaseinintracellularcalciumconcentration
causesvesicles(tinycontainersenclosedbyalipidmembrane)filledwithaneurotransmitterchemicalto
fusewiththeaxon'smembraneandemptytheircontentsintotheextracellularspace.The
neurotransmitterisreleasedfromthepresynapticnervethroughexocytosis.Theneurotransmitter
chemicalthendiffusesacrosstoreceptorslocatedonthemembraneofthetargetcell.The
neurotransmitterbindstothesereceptorsandactivatesthem.Dependingonthetypeofreceptorsthatare
activated,theeffectonthetargetcellcanbetoexcitethetargetcell,inhibitit,oralteritsmetabolismin
someway.Thisentiresequenceofeventsoftentakesplaceinlessthanathousandthofasecond.
Afterward,insidethepresynapticterminal,anewsetofvesiclesaremovedintopositionnexttothe
membrane,readytobereleasedwhenthenextactionpotentialarrives.Theactionpotentialisthefinal
electricalstepintheintegrationofsynapticmessagesatthescaleoftheneuron.[2]
Extracellularrecordingsofactionpotentialpropagationinaxonshasbeendemonstratedinfreely
movinganimals.Whileextracellularsomaticactionpotentialshavebeenusedtostudycellularactivity
infreelymovinganimalssuchasplacecells,axonalactivityinbothwhiteandgraymattercanalsobe
recorded.Extracellularrecordingsofaxonactionpotentialpropagationisdistinctfromsomaticaction
potentialsinthreeways:1.Thesignalhasashorterpeaktroughduration(~150s)thanofpyramidal
cells(~500s)orinterneurons(~250s).2.Thevoltagechangeistriphasic.3.Activityrecordedona
tetrodeisseenononlyoneofthefourrecordingwires.Inrecordingsfromfreelymovingrats,axonal
signalshavebeenisolatedinwhitemattertractsincludingthealveusandthecorpuscallosumaswell
hippocampalgraymatter.[6]
Infact,thegenerationofactionpotentialsinvivoissequentialinnature,andthesesequentialspikes
constitutethedigitalcodesintheneurons.Althoughpreviousstudiesindicateanaxonaloriginofa
singlespikeevokedbyshorttermpulses,physiologicalsignalsinvivotriggertheinitiationofsequential
spikesatthecellbodiesoftheneurons.[7][8]
Inadditiontopropagatingactionpotentialstoaxonalterminals,theaxonisabletoamplifytheaction
potentials,whichmakessureasecurepropagationofsequentialactionpotentialstowardtheaxonal
terminal.Intermsofmolecularmechanisms,voltagegatedsodiumchannelsintheaxonspossesslower
thresholdandshorterrefractoryperiodinresponsetoshorttermpulses.[9]

Developmentandgrowth
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Development
Studiesdoneonculturedhippocampalneuronssuggestthat
neuronsinitiallyproducemultipleneuritesthatareequivalent,
yetonlyoneoftheseneuritesisdestinedtobecometheaxon.[10]
Itisunclearwhetheraxonspecificationprecedesaxonelongation
orviceversa,[11]althoughrecentevidencepointstothelatter.If
anaxonthatisnotfullydevelopediscut,thepolaritycanchange
andotherneuritescanpotentiallybecometheaxon.This
alterationofpolarityonlyoccurswhentheaxoniscutatleast10
mshorterthantheotherneurites.Aftertheincisionismade,the
longestneuritewillbecomethefutureaxonandalltheother
neurites,includingtheoriginalaxon,willturnintodendrites.[12]
Imposinganexternalforceonaneurite,causingittoelongate,
willmakeitbecomeanaxon.[13]Nonetheless,axonal
developmentisachievedthroughacomplexinterplaybetween
extracellularsignaling,intracellularsignalingandcytoskeletal
dynamics.
Extracellularsignaling

A)pyramidalcell,interneuron,and
shortdurationwaveform(Axon).(B)
overlayofthethreeaverage
waveforms(C)averageandstandard
errorofpeaktroughtimefor
pyramidalcellsinterneurons,and
putativeaxons.(D)Scatterplotof
signaltonoiseratiosforindividual
unitsagainstpeaktroughtimefor
axons,pyramidalcells(PYR)and
interneurons(INT).

Theextracellularsignalsthatpropagatethroughtheextracellular
matrixsurroundingneuronsplayaprominentroleinaxonal
development.[14]Thesesignalingmoleculesincludeproteins,
neurotrophicfactors,andextracellularmatrixandadhesion
molecules.UNC6ornetrin,asecretedprotein,functionsinaxon
formation.WhentheUNC6receptorismutated,severalneurites
areirregularlyprojectedoutofneuronsandfinallyasingleaxonisextendedanteriorly.[15][16][17][18]The
neurotrophicfactorsnervegrowthfactor(NGF),brainderivedneurotrophicfactor(BDNF)and
neurotrophin3(NT3)arealsoinvolvedinaxondevelopmentandbindtoTrkreceptors.[19]
Thegangliosideconvertingenzymeplasmamembranegangliosidesialidase(PMGS),whichisinvolved
intheactivationofTrkAatthetipofneutrites,isrequiredfortheelongationofaxons.PMGS
asymmetricallydistributestothetipoftheneuritethatisdestinedtobecomethefutureaxon.[20]
Intracellularsignaling
Duringaxonaldevelopment,theactivityofPI3Kisincreasedatthetipofdestinedaxon.Disruptingthe
activityofPI3Kinhibitsaxonaldevelopment.ActivationofPI3Kresultsintheproductionof
phosphatidylinositol(3,4,5)trisphosphate(PtdIns)whichcancausesignificantelongationofaneurite,
convertingitintoanaxon.Assuch,theoverexpressionofphosphatasesthatdephosphorylatePtdIns
leadsintothefailureofpolarization.[14]
Cytoskeletaldynamics
Theneuritewiththelowestactinfilamentcontentwillbecometheaxon.PGMSconcentrationandf
actincontentareinverselycorrelatedwhenPGMSbecomesenrichedatthetipofaneurite,itsfactin
contentissubstantiallydecreased.[20]Inaddition,exposuretoactindepolimerizingdrugsandtoxinB
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(whichinactivatesRhosignaling)causestheformationofmultipleaxons.Consequently,theinterruption
oftheactinnetworkinagrowthconewillpromoteitsneuritetobecometheaxon.[21]

Growth
Growingaxonsmovethroughtheirenvironmentviathegrowthcone,whichis
atthetipoftheaxon.Thegrowthconehasabroadsheetlikeextensioncalled
lamellipodiawhichcontainprotrusionscalledfilopodia.Thefilopodiaarethe
mechanismbywhichtheentireprocessadherestosurfacesandexploresthe
surroundingenvironment.Actinplaysamajorroleinthemobilityofthis
system.EnvironmentswithhighlevelsofcelladhesionmoleculesorCAM's
createanidealenvironmentforaxonalgrowth.Thisseemstoprovidea"sticky"
surfaceforaxonstogrowalong.ExamplesofCAM'sspecifictoneuralsystems
includeNCAM,neuroglialCAMorNgCAM,TAG1,andMAGallofwhich
arepartoftheimmunoglobulinsuperfamily.Anothersetofmoleculescalled
extracellularmatrixadhesionmoleculesalsoprovideastickysubstratefor
axonstogrowalong.Examplesofthesemoleculesincludelaminin,fibronectin,
tenascin,andperlecan.Someofthesearesurfaceboundtocellsandthusactas
shortrangeattractantsorrepellents.Othersaredifusibleligandsandthuscan
havelongrangeeffects.

Axonof9dayold
mousewithgrowth
conevisible

Cellscalledguidepostcellsassistintheguidanceofneuronalaxongrowth.Thesecellsaretypically
other,sometimesimmature,neurons.
Ithasalsobeendiscoveredthroughresearchthatiftheaxonsofaneuronweredamaged,aslongasthe
soma(thecellbodyofaneuron)isnotdamaged,theaxonswouldregenerateandremakethesynaptic
connectionswithneuronswiththehelpofguidepostcells.Thisisalsoreferredtoas
neuroregeneration.[22]
NogoAisatypeofneuritegrowthinhibitorycomponentthatispresentinthecentralnervoussystem
myelinmembranes(foundinanaxon).Ithasacrucialroleinrestrictingaxonalregenerationinadult
mammaliancentralnervoussystem.Inrecentstudies,ifNogoAisblockedandneutralized,itis
possibletoinducelongdistanceaxonalregenerationwhichleadstoenhancementoffunctionalrecovery
inratsandmousespinalcord.Thishasyettobedoneonhumans.[23]Arecentstudyhasalsofoundthat
macrophagesactivatedthroughaspecificinflammatorypathwayactivatedbytheDectin1receptorare
capableofpromotingaxonrecovery,alsohowevercausingneurotoxicityintheneuron.[24]

History
Someofthefirstintracellularrecordingsinanervoussystemweremadeinthelate1930sbyKennethS.
ColeandHowardJ.Curtis.GermananatomistOttoFriedrichKarlDeitersisgenerallycreditedwiththe
discoveryoftheaxonbydistinguishingitfromthedendrites.[2]SwissRdolfAlbertvonKllikerand
GermanRobertRemakwerethefirsttoidentifyandcharacterizetheaxoninitialsegment.AlanHodgkin
andAndrewHuxleyalsoemployedthesquidgiantaxon(1939)andby1952theyhadobtainedafull
quantitativedescriptionoftheionicbasisoftheactionpotential,leadingtheformulationofthe
HodgkinHuxleymodel.HodgkinandHuxleywereawardedjointlytheNobelPrizeforthisworkin
1963.TheformulasdetailingaxonalconductancewereextendedtovertebratesintheFrankenhaeuser
Huxleyequations.LouisAntoineRanvierwasthefirsttodescribethegapsornodesfoundonaxonsand
forthiscontributiontheseaxonalfeaturesarenowcommonlyreferredtoastheNodesofRanvier.
SantiagoRamnyCajal,aSpanishanatomist,proposedthataxonsweretheoutputcomponentsof
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neurons,describingtheirfunctionality.[2]ErlangerandGasserearlierdevelopedtheclassificationsystem
forperipheralnervefibers,[25]basedonaxonalconductionvelocity,myelination,fibersizeetc.Even
recentlyourunderstandingofthebiochemicalbasisforactionpotentialpropagationhasadvanced,and
nowincludesmanydetailsaboutindividualionchannels.

Injury
Inorderofdegreeofseverity,injurytoanervecanbedescribedasneuropraxia,axonotmesis,or
neurotmesis.Concussionisconsideredamildformofdiffuseaxonalinjury.[26]Thedysfunctionof
axonsinthenervoussystemisoneofthemajorcausesofmanyinheritedneurologicaldisordersthat
affectbothperipheralandcentralneurons.[2]

Classification
Theaxonsthatmakeupnervesinthehumanperipheralnervoussystemcanbeclassifiedbasedontheir
physicalfeaturesandsignalconductionproperties.

Motor
Lowermotorneuronshavetwokindoffibers:
Motorfibertypes
Type

ErlangerGasser
Diameter(m) Myelin Conductionvelocity Associatedmusclefibers
Classification

1320

Yes

80120m/s

Extrafusalmusclefibers

58

Yes

424m/s[27][28]

Intrafusalmusclefibers

Sensory
Differentsensoryreceptorsareinnervatedbydifferenttypesofnervefibers.Proprioceptorsare
innervatedbytypeIa,IbandIIsensoryfibers,mechanoreceptorsbytypeIIandIIIsensoryfibersand
nociceptorsandthermoreceptorsbytypeIIIandIVsensoryfibers.

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Sensoryfibertypes
Erlanger
Type
Gasser
Classification

Diameter
(m)

Conduction
velocity

Myelin

Associatedsensoryreceptors

Ia

1320

Yes

80120m/s

Primaryreceptorsofmusclespindle

Ib

1320

Yes

80120m/s

Golgitendonorgan

3375m/s

Secondaryreceptorsofmuscle
spindle
Allcutaneousmechanoreceptors

II

612

Yes

III A

15

Thin

330m/s

Freenerveendingsoftouchand
pressure
Nociceptorsofneospinothalamic
tract
Coldthermoreceptors

IV C

0.21.5

No

0.52.0m/s

Nociceptorsofpaleospinothalamic
tract
Warmthreceptors

Autonomic
Theautonomicnervoussystemhastwokindsofperipheralfibers:

Type

Fibertypes
ErlangerGasser
Diameter(m) Myelin[29] Conductionvelocity
Classification

preganglionicfibers B

15

Yes

315m/s

postganglionicfibers C

0.21.5

No

0.52.0m/s

Seealso
Axonguidance
Electrophysiology
Nervefiber
Pioneeraxon
Telodendron

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Externallinks
Histologyimage:3_09(http://www.ouhsc.edu/histology/Glass%20slides/3_09.jpg)atthe
UniversityofOklahomaHealthSciencesCenter"Slide3Spinalcord"
Bialowas,Andrzej,Carlier,Edmond,Campanac,Emilie,Debanne,Dominique,Alcaraz.Axon
Physiology,GislePHYSIOLOGICALREVIEWS,V.91(2),04/2011,p.555602.
(http://physrev.physiology.org.myaccess.library.utoronto.ca/content/91/2/555)
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Categories: Neurons Neurophysiology Neuroanatomy
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