Ill
However, in view of our results and others (Nagata et al.,
1986) which indicate that A2B5 antigen may be modulated by
loss of neuronal contact it seems possible that its
expression on the surface of type 2 astrocytes may also be
in response to neuronal deprivation. This would occur when
the optic nerve was dissected as only axons are present
there. By the time that the nerve is dissociated and the
cells are plated several hours would have passed which in
my system is ample time for many A2B5(-) cells to express
the antigen on their surfaces (data not shown). This
possibility would not be easy to rule out since I and
others (Schnitzer and Schachner, 1982; Dr. M.F.Marusich,
personal communication) have found that all neural cells,
including glia, contain intracellular epitopes for A2B5.
This last point precludes the usefulness of A2B5 as a
neuronal marker in tissue that was first fixed and
permeablized before incubation in A2B5, such as in tissue
sections.
Explanation of Abnormal Phenotypes
The phenotypes that appeared in purified cultures such
as A2B5(+)/5A11(+) round cells, NF-M(+) flat cells, and
A2B5(+)/GFAP(+) flat cells were clearly abnormal. These
markers that were co-localized in purified cultures were
always segregated into different cells in unpurified
cultures. The possibility that these abnormal phenotypes
were generated as a result of the procedure itself seems