Wallerian degeneration

This article is part of a series created to help myself learn Neurobiological concepts and develop my scientific writing. I intend to write one entry everyday, or if not, at least 3 a week. My objective is to make an interesting reading, comprehensible, but scientifically accurate (I don't want to delve so much into a "divulgating style" that it wouldn't be interesting for a biology student). I hope you like my project!

Wallerian degeneration

Wallerian degeneration is the process of axon degeneration, distal to a site of transection. It can take place in the peripheral nervous system (PNS) and in the central nervous system (CNS), but the process is different in each of these systems.

PNS: After a peripheral nerve transection, the distal axon starts to degenerate. Macrophages come into the nerve and remove myelin and axonal debris. The Schwann cells and the basement membrane around the axon remain there, but Schwann cells undergo a change in their shape, which allows them to start secreting neurotrophic factors, that favour axon growth. The basement membrane and the Schwann cells are creating "tunnels" that go directly to the muscle that has lost innervation. Axons proximal to the injury site might start sending axonal growth cones that are attracted to Schwann cells-secreted neurotrophic factors. If these axons enter one of the aforementioned "tunnels", then they will probably be capable of arriving to the target muscle, reinnervating it. Although, this reinervation is not usually done in the same way that it was before, and therefore, regeneration of peripheral nerves might entail a certain loss of function (because of a motoneuron innervating a wrong group of muscle fibers -too big or too small for it-, because of a bad growth, because of insufficient reinervation,...) or other related conditions. After this axonal growth, Schwann cells remyelinate these axons; the newly formed axons can be recognized for having a thinner myelin cover, and shorter-than-usual internodes.

CNS: Wallerian degeneration in the CNS can be seen in spinal cord trauma -I guess Wallerian degeneration is by definition possible in the brain (there are also axons in the brain), but I've got the feeling that it is just applied to the spinal cord; probably because in the brain, proximal and distal terms are not so clear; anyway, a Wallerian degeneration in the brain would probably look quite different than Wallerian degeneration after spinal cord trauma-. Spinal cord injure courses with: 1) a contusion/bruise at the site of injury, 2) a cone of hemorragic necrosis in the central section of the cord, extending several centimetres above and below the site of injury, 3) Wallerian degeration of the axons distal to the site of injury: macrophages remove debris for 2-4 weeks, and astrocytes (GFAP positive cells), proliferate largely and cover the distal axons, 4) this "astrocyte scar" is thought to be guilty of the loss of capacity of spinal cord nerves to regenerate, the GFAP scar avoids axon regeneration into the distal section.

Source: http://missinglink.ucsf.edu/lm/ids_104_cns_injury/response%20_to_injury/walleriandegeneration.htm

Three different types of lesion of the peripheral nerve:

- Neuropraxia or axonopraxia: interruption of neural conduction without proof of nerve damage. There is no Wallerian degeneration.

- Axonotmesis: only the axons are injured, and connective sheats of the nerve are preserved (endoneurium, perineurium and epineurium). Regeneration is common and functional recovery is usually good.

- Neurotmesis: endoneurial tubes loss their continuity. Repair is possible, but aberrant connectivity after the injury is common. In this case, axon-target reconnection is not specific, and thus, it is usually incorrect.

Sources: http://es.wikipedia.org/wiki/Lesi%C3%B3n_de_nervio#Axonotmesis and the article wich this entrance is based at: Allodi I, Udina E and Navarro X. Specificity of peripheral nerve regeneration: Interactions at the axon level. Prog in Neurobiol. 2012; 98: 16-37.