Universlty of Manitoba, ln Partîal Fulfiìlment - MSpace at the ...

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took up the label, shovri.ng thêt differentiation had not yet occurred
(l'lart I n and Langman, 1965).
ln splotch and looptê¡ I mice the development of open neural defects
(which are a major expressîon of the mutant genes) is accompanied by a
prolonged cell cycle in the neuroe p ithelium, and an accumulatlon of
mitotic figures. This retardation îs followeó by a pericd of accelerated
cel I divislon, producing oúergrowth of the open neural tissue (Hsu and
Van Dyke, 1948; ì,/¡lson, t974; 1974). ln trypan blue - induced dysraphlsm
of rat enbryos, autoradiography at l0| days provided no evidence of lncreased
mltosls ln the neural tube (Lendon, l!/2).
Reductlon of mltosis, however, may not be essential to the development
of neural dysraphlsm. Davis (t942, 1944) found that in neural
dysraphîsm of chick embryos produced by ultraviolet irradiation, the
wavelengths that were most effective in reducing mitoses in the neural
plate were least effectíve in inhibitíng neurulation.
ln the present chick embryos m¡totic figures appeared to be restricted
to the exposed plaq,ue surface and the luminal surface of closed areas in
myeloschîsis; figures were more scattered through the ta¡ l-bud material in
nryelodysplasia. 14Ítotic dens¡ties in these lesions were not estimated
because the séparation of neural tissue into its two sources of origln
made ít impossible to count figures in relation to a constant sur.face area.
lilany of the changes associated wîth the development of open neural
defects in windowed chick embryos are relevant to the pathogenesis of
dysraphism in man. ln the human developmental horizons formulated by
Streeter (1942), the anter¡or neuropore closes during horlzon Xl (,l3-20
somites) and posterior neuropore during horlzon Xll (2.|-29 somites).
ln the chlck embryo the anterior neuropore closes at Stage ll (,|3 somites)