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

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The inpresslon of somlte separât¡on in embryos wlth myeloschisis
was not confirned by further analysis, as the lengths of somite separatîon
dld not correspond to the revers of the defects, and extensîve somite
separation occurred in control embryos.
ln , aaurans (with a bilaminar neural plate), analysis of the mech_
anlsm of neurulatlon revears that as well as'lntrinsic forces within the
neural plate, folding involves elevation of the differentlatlng somites,
ln the presence oi tight adhesion between neural plate and notochord
(Schroeder, 1!/0). Somite elevation does not appear to be împortant ln
the chick embryo, as disruptron of neuroepither iar mîcrotubures (by corchrcine)
and mlcrofllaments (by cytochalasin B) înhiblts or even reverses neurulation
(Karfunkel , 1972).
ln mammals, open neural defects have been produced by maternal
treatment wlth varlous agents, încludíng trypan blue ln rats (Gillman et
al., 1948; l,/arkany et ai., l95B; Lendon, t96gt 1915; Rokos et al., t97O;
1976| or mice (tJaddington ênd Carrer, 1953; Hamburgh, 1954): and dímethyl
sulfoxlde or high doses of vrtamin A in hamsters (Marin-padi a and Ferm,
1965; Marin-Padilla, r966; 1966; Ferm t966). rn each cêse rhe development
of the neural defects was crosery associated with edema, cyst formâtion,
and hemorrhages in local mesoderm. Rokos et al. (,|970) also descríbed
extensive cell death ín mesoderm, heart, gut and neural plate.
ln embryos recoùered within 48 hours of maternal injection with
vitamin A or dimethyl sulfoxide, accumulation of f .luld and dilation of
local slnusoids was observed in unsegmented nesoderm at g-10 hours, followed
by necrosis and col lapse of somítes after 24 hours (l4arin-padil la and