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

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. These findings s.ugges r that myelodysplasia does not ar¡se by simple
non-closure of the neural folds, but develops from the tail-bud materiar
after St¿ge 15, in the absence of neural plate materlal.
Histologically, deveropment of the rhombic roof showed no difference
ln enbryos wi th and wÌthout neurar defects. The choroid prexuses did not
âppear unt¡l Stage rB in either control or experîmental embryo, after the
establ lshment of myeloschisis and nryeIodyspIasIa. rn these wlndowed chick
embryos, open neural defects cannot be attrlbuted to delayed passage of
cerebro-splnal fluld across the rhombic roof as suggested by Gardner (r!6r,
1964, 1972).
The role played by the ¡14çip¡¡L in neurulation ls stl I I not clear,
desplte many investigat¡ons. Elongation of the notochord appears to be
an essential componen t of neural plate formation (Holtfreter,
1955). Jacobson and Gordon (1976) snowe¿ by cell counts in Tri turus
that the extending notochord does not creave through the neurar prate
cells, but dísplaces them anterîorly to contrlbute to the future brain.
ln several mutant mice such as Danforthrs short taí1, brachyury,
anury and trgncête, open and closed neural defects occur sporadical ly,
but are probab.l y secondary to abnormarities of the notochord or pr¡m¡tive
streak (Grüneberg, rg63). These mutants show extensive vertebrar defects
of the splne and tail, as well as some vîsceral defects, "rro"i"t"d
*¡th
the notochordal malformatîons. Thei r neurar defects may represent myerodysplas
ia rather than nryeloschisis.
The slze of the notochord is reduced in amphibia by treatment wrth
l¡thlum chlorlde (Lehmann, 1937), and enlarged by treêtmeñt wÍth sodium
thlocyanate (Ranzri and Tanlnl, 1939). These changes can be explained by
act¡on of the postulated mesodeimal¡z¡ng factor (Tolvonen, l96l; Tolvonen