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the appearance of A2B5 antigen on purified cell surfaces is
not due to the modification of existing gangliosides on the
surface or even intracellularly. This cannot be ruled out,
however, because increases in the complex gangliosides
(including GQic) during development of the chick optic
tectum are correlated with decreases in simpler precursors
(Gd3) (Rosner, 1980). Other possibilities that may explain
the appearance of A2B5 antigen are new synthesis and export
to the surface, or export of an intracellular pool. Since
it is known that chick brain cells have intracellular pools
of A2B5 antigen (see below; Schnitzer and Schachner, 1982)
this possibility is quite real. Export to the surface
could be via exocytotic vesicles or via a ganglioside
transfer protein found in brain (Gammon and Ledeen, 1985).
These types of export mechanisms could account for the
appearance of A2B5 antigen on the surfaces of purified
cells within the several hours that it has been seen to
occur (see Results).
The number of "recruited A2B5(+) cells was a function
of the number of original A2B5(+) cells that were removed
as demonstrated by the calculated incomplete separations.
The question remains as to whether this triggered
modulation of A2B5 antigen was a result of the removal of
neurons or of A2B5(+) cells. Some (20%) of the A2B5(+)
cells that were removed are known to be neurons because
they contained neurofilaments. The remaining 80% were of