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unknown type. They may, however, have been neurons that
either did not contain neurofilaments because of lack of
synthesis in the tissue or because of severing of axons
during dissociations. The results of culturing cells
recovered from the microspheres on glass and polyornithine
suggest that these are neurons because cultures from these
A2B5(+)-enriched cells appeared to be neuron-enriched.
Later on, there was a tight correlation between a cell
being A2B5(+) and having a neuronal morphology in long-term
monolayer cultures. Therefore, modulation of A2B5 antigen
on purified A2B5(-) cell surfaces may be a response to
neuronal depletion as effected by the removal of A2B5(+)
cells. Consistent with this hypothesis, surface A2B5
antigen modulation has been shown to occur with mouse
cerebellar astrocytes in culture in response to complement-
mediated depletion of neurons using an independent neuronal
marker (Nagata et al., 1986).
The inability to prevent recruitment of new A2B5(+)
cells by mixing back the cells that were removed implies
that the recruitment was very rapid and irreversible. There
exists the possibility that this was due to damage of the
cells that were removed from the microspheres by the second
trypsinization. This seems unlikely, however, since the
cells were trypsinized before dissociation. These recovered
cells also grew well in culture. It appears that the
events that led to the expression of A2B5 antigen on the