Prior collateral sprouting enhances elongation rate of sensory axons regenerating through acellular distal segment of a crushed peripheral nerve

Citation
F. Bajrovic et al., Prior collateral sprouting enhances elongation rate of sensory axons regenerating through acellular distal segment of a crushed peripheral nerve, J PERIPH N, 4(1), 1999, pp. 5-12
Citations number
52
Categorie Soggetti
Neurosciences & Behavoir
Journal title
JOURNAL OF THE PERIPHERAL NERVOUS SYSTEM
ISSN journal
10859489 → ACNP
Volume
4
Issue
1
Year of publication
1999
Pages
5 - 12
Database
ISI
SICI code
1085-9489(1999)4:1<5:PCSEER>2.0.ZU;2-S
Abstract
Regenerating axons in crushed peripheral nerves grow through their distal n erve segments even in the absence of Schwann cell support, but their elonga tion rate is reduced by 30%. We examined whether prior exposure of sensory neurons to trophic factors achieved either by collateral sprouting or regen eration after conditioning lesion could enhance subsequent regeneration of their axons after crush, and compensate for loss of cell support. Collatera l sprouting of the peroneal cutaneous sensory axons in the rat was evoked b y transection of adjacent peripheral nerves in the hind leg. The segment of the peroneal nerve distal to the crush was made acellular by repeated free zing. Sensory axon elongation rate during regeneration was measured by the nerve pinch test. Prior axonal sprouting for two weeks increased the elonga tion rate of sensory axons through the acellular distal nerve segment back to normal value observed in control crushed nerves. The number of axons in the acellular distal segment at a fixed distance from the crush site was ab out 50% greater in sprouting than in control non-sprouting nerves. However, prior sprouting caused no further increase of axon elongation rate in cont rol crushed nerves. Prior collateral sprouting, therefore, could in some re spect compensate for loss of cell support in the distal nerve segment after crush lesion. This suggests that loss of cell-produced trophic factors is probably responsible for slower elongation rate through the acellular dista l nerve segment. Surprisingly, prior conditioning lesion caused no enhancem ent of elongation rate of the sensory axons regenerating in the absence of cell support.