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culture (80%) far surpasses the levels in unpurified
cultures (45%). This suggests that the population of
reactive cells is not taken from a resting blast
population, as it is unlikely that more resting blast cells
would be present after the phases of proliferation and
migration within the tectum have ceased (LaVail and Cowan,
1971a,b) than during the proliferative phase.
Alternatively, blast cells may have been released more
easily from the tissue during dissociation than were
differentiating cells. More importantly, since >90% of the
purified cells were identified as definitive glia already
expressing differentiation markers the reactive population
must have come largely from definitive glia. This also
demonstrates that, in the chick system, A2B5 antigen on the
surfaces of glia was induced experimentally. And since the
GC(+) cells in the purified population did not become
A2B5(+) it appears that the reactive cells are wholly of
the astrocyte lineage. Lastly, it is worth noting that none
of the recruited A2B5(+) cells incorporated 3H-thymidine.
This clearly demonstrated that new DNA synthesis, and hence
mitosis, was not required for A2B5 antigen modulation.
Possible explanations of the mechanisms that may be
operating to effect this change in phenotype are given in
the Discussion section in Chapter II.