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

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1962i 1965). Barth and Barth.(1974) susgest that inducing ðgents may
act by aliering the propertles of cell membranes in the reactî.ng tìssue,
to promote red¡str¡bution of intracellular ions.
Fai lure of înductiori might, occur byl restriction of contêct
between the two interacting t¡ssues; a defect in the înductor; incompetence
of the reacting tissue; or imperfect tíming of the contact
between the two t¡ssue components (Saxá, 1975).
Cell death occurs as a normal phenomenon in many embryoníc processes'
part¡cuìarly those involvîng morphogenesis or regression (Glucksmann, 1951) '
Regressive phases ln embryogenesis are programmed to occur in a specifíc
sequence that suggests genetic control. Mutant genes cên enhance or
reduce the normal patterns of celì death (Saunders, 1966) ' Experimental
treatments such as x-rays' drugs, viruses, hormones, vitamins, and hypoxla
can promote cell death (l4enkes et al. 1970); Janus green can Prevent the
normal cell death in the interdÎgital clefts of the chíck foot (Saunders,
r966).
Necrobiosis in the neural tube shows peaks preceding neural groove
formatíon, foldîn9, fusion, and separatíon îrom surface ectoderm
(Glucksmann, l95l). Käl lén (1955) des.cribed another peak of cell deaths
ln the rabbí t brain, associated with a period of ce'l I differentîatíon at
14 days, Rokos et ê1. (1976) described cell deaths in mesoderm,'heart,
gut, and neural plate tissues of rat embryos after maternal injection of
trypan blue; they suggested that th¡s was an exaggerated form of the nor-
¡na I cell death seen in early neurogenesis.
Cell death is accompanled at early embryonic stêges by a ttj!h-regu-.
.làtli¿è àbititv, which is responsîble for rapid lncorporation of grafts