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must have come from preexisting nonneuronal cells to
exhibit the same density as in unpurified cultures (see 3H-
thymidine discussion below). The simplest explanation for
equal densities of neurons is that A2B5 expression on the
surfaces of cells is irrelevant to the development of
neurons in long-term monolayer cultures. A2B5 antigen may
have been modulated up and down on cell surfaces in both
unpurified and purified cultures. Then, the A2B5(+) neurons
at the culture endpoints may not have developed from the
A2B5(+) cells seen initially or after a day in culture. The
phenomenon of recruitment of A2B5(+) cells in purified
cultures may be separate from the appearance of neurons in
these cultures. No experiments were performed that could
conclusively demonstrate which of the possibilities had
occured.
On the other hand, neurons as defined by morphology
and/ or neurofilament content were almost always surface
A2B5(+) (>90%) in long-term monolayer cultures. Conversely,
cells that expressed A2B5 antigen on their surfaces always
had a neuronal morphology in monolayer cultures.
Additionally, the presence of cells that were surface
A2B5(+) always preceded the development of neurons in long
term cultures. A2B5(+) cells were present at the outset in
unpurified cultures, and were present after one day in
purified cultures. These correlations raise the possibility
that A2B5(+) neurons in long-term cultures developed from