Editing Neuron (section)

===Axonal degeneration===
Although most injury responses include a calcium influx signaling to promote resealing of severed parts, axonal injuries initially lead to acute [[axonal degeneration]], which is the rapid separation of the proximal and distal ends, occurring within 30 minutes of injury.<ref name="NM">{{cite journal | vauthors = Kerschensteiner M, Schwab ME, Lichtman JW, Misgeld T | s2cid = 25287010 | title = In vivo imaging of axonal degeneration and regeneration in the injured spinal cord | journal = Nature Medicine | volume = 11 | issue = 5 | pages = 572–7 | date = May 2005 | pmid = 15821747 | doi = 10.1038/nm1229 }}</ref> Degeneration follows with swelling of the [[axolemma]], and eventually leads to bead-like formation. Granular disintegration of the axonal [[cytoskeleton]] and inner [[organelle]]s occurs after axolemma degradation. Early changes include accumulation of [[mitochondria]] in the paranodal regions at the site of injury. The endoplasmic reticulum degrades and mitochondria swell up and eventually disintegrate. The disintegration is dependent on [[ubiquitin]] and [[calpain]] [[proteases]] (caused by the influx of calcium ions), suggesting that axonal degeneration is an active process that produces complete fragmentation. The process takes about roughly 24 hours in the PNS and longer in the CNS. The signaling pathways leading to axolemma degeneration are unknown.