THE PATTERN OF AXONAL DEGENERATION IN THE PERIPHERAL NERVOUS-SYSTEM VARIES WITH DIFFERENT TYPES OF LESION

Degeneration of axons in the mouse sciatic nerve was examined using conventional silver staining and by noting the presence or absence of a compound action potential on stimulating the nerve distal to the point of crush or cut. The presence of myeloperoxidase-positive cells was also examined in frozen sections of the nerve. In all experiments the distal, disconnected segment was studied. Degeneration after crushing with fine watchmakers forceps always began in the most distal part of the nerve and proceeded in a distoproximal direction, from the nerve entry point into a muscle back to the crush site. Myeloperoxidase-positive cells were also recruited into the nerve starting at the distal rather than proximal (the originally injured) end. This result favours the view that degeneration is triggered by lack of trophic support from the cell body rather than entry of deleterious substances at the site of the injury, for the terminals furthest from both the source of supply and the injury are affected first. Degeneration following nerve section was always more rapid than after crushing. The rate of axonal sealing at the injury was, however, no slower than after crushing, so it does not seem likely that greater entry of possible degeneration-triggering material at the injury site is the explanation for this. Crush lesions in which the perineurium was also cut open and the blood supply at the site was damaged, degenerated at the slower rate characteristic of simple crushes. Hence, it does not seem likely that perineurial or vascular damage, both of which are much more extensive following nerve section, provide an explanation for the more rapid degeneration of cut nerves. If a sufficiently large length of sciatic was frozen or if it was ligatured with fine silk, degeneration was as rapid as after nerve section, while, if a ligature was immediately untied, degeneration was as slow as that following crush with forceps. It is concluded that continuing contact of the distal with the proximal nerve stump slows degeneration, possibly by allowing Schwann cells above and below the lesion to continue communicating or by providing a minimal supply of trophic material. © 1990.