Editing Axon (section)

===Growth===
{{Main|Axon guidance}}
[[File:Axon two photon.jpg|thumb|right|upright|Axon of nine-day-old mouse with growth cone visible]]
Growing axons move through their environment via the [[growth cone]], which is at the tip of the axon. The growth cone has a broad sheet-like extension called a [[lamellipodium]] which contain protrusions called [[filopodia]]. The filopodia are the mechanism by which the entire process adheres to surfaces and explores the surrounding environment. Actin plays a major role in the mobility of this system. Environments with high levels of [[cell adhesion molecule]]s (CAMs) create an ideal environment for axonal growth. This seems to provide a "sticky" surface for axons to grow along. Examples of CAMs specific to neural systems include [[Neural cell adhesion molecule|N-CAM]], [[Contactin 2|TAG-1]]{{Snd}}an axonal [[glycoprotein]]<ref name="Furley">{{cite journal | vauthors = Furley AJ, Morton SB, Manalo D, Karagogeos D, Dodd J, Jessell TM | title = The axonal glycoprotein TAG-1 is an immunoglobulin superfamily member with neurite outgrowth-promoting activity | journal = Cell | volume = 61 | issue = 1 | pages = 157–70 | date = April 1990 | pmid = 2317872 | doi = 10.1016/0092-8674(90)90223-2 | s2cid = 28813676 | doi-access = free }}</ref>{{Snd}}and [[Myelin-associated glycoprotein|MAG]], all of which are part of the [[immunoglobulin]] superfamily. Another set of molecules called [[extracellular matrix]]-[[cell adhesion molecule|adhesion molecule]]s also provide a sticky substrate for axons to grow along. Examples of these molecules include [[laminin]], [[fibronectin]], [[tenascin]], and [[perlecan]]. Some of these are surface bound to cells and thus act as short range attractants or repellents. Others are difusible ligands and thus can have long range effects.

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>

[[Reticulon 4|Nogo-A]] is a type of neurite outgrowth inhibitory component that is present in the central nervous system myelin membranes (found in an axon). It has a crucial role in restricting axonal regeneration in adult mammalian central nervous system. In recent studies, if Nogo-A is blocked and neutralized, it is possible to induce long-distance axonal regeneration which leads to enhancement of functional recovery in rats and mouse spinal cord. This has yet to be done on humans.<ref>{{cite journal | vauthors = Schwab ME | title = Nogo and axon regeneration | journal = Current Opinion in Neurobiology | volume = 14 | issue = 1 | pages = 118–24 | date = February 2004 | pmid = 15018947 | doi = 10.1016/j.conb.2004.01.004 | s2cid = 9672315 }}</ref> A recent study has also found that [[macrophage]]s activated through a specific inflammatory pathway activated by the [[CLEC7A|Dectin-1]] receptor are capable of promoting axon recovery, also however causing [[neurotoxicity]] in the neuron.<ref>{{cite journal | vauthors = Gensel JC, Nakamura S, Guan Z, van Rooijen N, Ankeny DP, Popovich PG | title = Macrophages promote axon regeneration with concurrent neurotoxicity | journal = The Journal of Neuroscience | volume = 29 | issue = 12 | pages = 3956–68 | date = March 2009 | pmid = 19321792 | pmc = 2693768 | doi = 10.1523/JNEUROSCI.3992-08.2009 }}</ref>