Vesicles and/or other membranous structures that form after
axolemmal damage have recently been shown to repair (seal)
the axolemma of various nerve axons. To determine the origin
of such membranous structures, (1) we internally dialyzed isolated
intact squid giant axons (GAs) and showed that elevation
of intracellular Ca21 .100 uM produced membranous structures
similar to those in axons transected in Ca21-containing
physiological saline; (2) we exposed GA axoplasm to Ca21-
containing salines and observed that membranous structures
did not form after removing the axolemma and glial sheath but
did form in severed GAs after .99% of their axoplasm was
removed by internal perfusion; (3) we examined transected GAs
and crayfish medial giant axons (MGAs) with time-lapse confocal
fluorescence microscopy and showed that many injuryinduced
vesicles formed by endocytosis of the axolemma; (4)
we examined the cut ends of GAs and MGAs with electron
microscopy and showed that most membranous structures
were single-walled at short (5–15 min) post-transection times,
whereas more were double- and multi-walled and of probable
glial origin after longer (30–150 min) post-transection times; and
(5) we examined differential interference contrast and confocal
images and showed that large and small lesions evoked similar
injury responses in which barriers to dye diffusion formed amid
an accumulation of vesicles and other membranous structures.
These and other data suggest that Ca21 inflow at large or small
axolemmal lesions induces various membranous structures (including
endocytotic vesicles) of glial or axonal origin to form,
accumulate, and interact with each other, preformed vesicles,
and/or the axolemma to repair the axolemmal damage.This work was supported by grants from National Institutes of Health (NIH;
NS31256) and the State of Texas (Advanced Technology 3658-446).Neuroscienc
