Single vs multiple somatic nerve crushes in the rat

Abstract

Nerve lesions modify regenerative responses to subsequent lesions. Some of the modifications might be useful. To increase our understanding of these modifications, the present study determines myelinated and unmyelinated axon numbers in the distal part of rat sciatic nerve and in 2 smaller branches, the nerve to the medial gastrocnemius muscle and the sural nerve, 8 weeks and 9 months following either single or the last of 3 crushes to the rat sciatic nerve. For myelinated axons, there is a significant and proportional increase distal to the crush in the sciatic nerve and in its smaller tributaries following both single and triple crushes. These increased axons persist. We interpret these data to indicate that some of the regenerating myelinated axons branch at the site of lesion, pass without branching into the tributary nerves, and then presumably find attachments at the periphery. If true, single or multiple crushes might be useful in conditions where it would be desirable to increase numbers of processes from surviving neurons. The major differences between single and triple crushes are that myelinated axons are increased more after triple crush and increase significantly between 8 weeks and 9 months after triple crush but not after single crush. Thus not only myelinated axon numbers, but the timing of the myelination process seems to change if regeneration following single crush is compared to similar regeneration following multiple crushes. Unmyelinated axons do not regenerate in the same way as the myelinated axons. The major difference is that unmyelinated axon numbers return to normal after long-term regeneration following either single or multiple crushes. The regeneration pattern differs, however, in that after 3 crushes and after single crush for the nerve to the medial gastrocnemius muscle, there is overproduction of axons followed by a return to normal levels, whereas for the sciatic and sural nerves after single crush, axon numbers slowly rise to normal levels. In the first case, therefore, there seems to be excess axon branching followed by a loss presumably due to the lack of formation of peripheral connections, whereas for the second case, there is no evidence of branching but only a steady increase to normal levels.