Introduction - Axon growth and axon regeneration are complex processes
requiring an adequate supply of certain metabolic precursors and nutr
ients. Material and methods - This article reviews the studies examini
ng some of the processes of protein modification fundamental to both n
erve regeneration and to the continuous and adequate supply of specifi
c factors such as arginine, S-adenosylmethionine and polyamines. Resul
ts - The process of arginylation notably increases following nerve inj
ury and during subsequent regeneration of the nerve, with the most lik
ely function of arginine-modification of nerve proteins being the degr
adation of proteins damaged through injury. It appears that defective
methyl group metabolism may be one of the leading causes of demyelinat
ion, as suggested by the observation of reduced cerebrospinal fluid co
ncentrations of s-adenosylmethionine (SAMe) and 5-methyltetrahydrofola
te, the key metabolites in methylation processes, in patients with a r
eduction in myelination of corticospinal tracts. Polyamine synthesis,
which depends strongly on the availability of both SAMe and arginine,
markedly increases in neurons soon after an injury. This ''polyamine-r
esponse'' has been found to be essential for the survival of the paren
t neurons after injury to their axons. Polyamines probably exert their
effects through involvement in DNA, RNA and protein synthesis, or thr
ough post-translational modifications that are indicated as the most r
elevant events of the ''axon reaction.'' Conclusions - Nerve regenerat
ion requires the presence of arginine, s-adenosylmethionine, and polya
mines. Further studies are needed to explore the mechanisms involved i
n these processes.