The poor regenerative ability of neurons of the central nervous system
in mammals, as compared with their counterpart in fish or amphibians,
is thought to stem from differences in their immediate nonneuronal en
vironment and its response to axonal injury. We describe one aspect of
the environmental response to axonal injury in a spontaneously regene
rating system-the fish optic nerve. The aspect under investigation was
the reaction of glial cells at the injury site. This was examined by
the use of antibodies that specifically recognize vimentin in fish gli
al cells. In the present study, affinity-purified vimentin antibodies
were raised against a nonconserved N-terminal 14-amino acid peptide, w
hich was predicted from the nucleotide sequence of vimentin. These ant
ibodies were found to react specifically with glial cells in vitro. Mo
reover, the antivimentin antibodies stained both the optic nerve and t
he optic tract, but with different patterns. Specificity of the antibo
dies was verified by protein immunoblotting, tissue distribution, and
labeling patterns. After injury, vimentin immunoreactivity initially d
isappeared from the site of the lesion due to cell death. Early signs
of glial cell migration toward the injury site were evident a few days
later. It is suggested that the reappearance of vimentin-positive gli
al cells at the site of injury is associated with axonal elongation ac
ross it, and that they contribute to the regenerative ability of the f
ish optic nerve. (C) 1994 Wiley-Liss, Inc.