The Kinase C Substrate Protein B-50 (GAP43) and its Function in Axonal Repair Mechanisms

Abstract

Severing of a nerve is accompanied by an assortment of morphological and biochemical changes in the neuronal cell bodies, the axonal processes and in the neuronal interstitium. In the peripheral nervous system (PNS) axons normally respond to damage by axonal regeneration, while in the central nervous system (CNS) axons generally regenerate poorly or not at all. The successful regeneration of axons appears to be dependent on the establishment of a neuronal micro-environment which is favorable for axonal regrowth. The importance of trophic factors and extracellular surface components in sustained axonal regrowth has been demonstrated widely (Berg 1984). The difference in the regenerative capacities of CNS and PNS neurons seems largely based on the failure of CNS tissue to provide the damaged axon with a milieu appropriate for axonal regeneration. This has, for instance, been shown in experiments in which damaged CNS axons were exposed to grafts of sciatic nerve tissue. One month after implantation of these PNS grafts, a large number of CNS axons had grown into the graft for distances of 3 cm or more. In the absence of the PNS graft the severed CNS axons would only have exhibited some abortive sprouting (Aguayo et al. 1982). Thus, CNS axons are not necessarily unable to regenerate, but it seems that the CNS environment is not permissive for axonal sprout formation.