Serial sections of embryonic rat eyes were stained with hematoxylin and eosin, quantified (by counting pycnotic and viable nuclei), reproduced by camera lucida on wax plates, and moulded into reconstructions in order to study the normal progression of cellular death during morphogenesis. At least nine distinct necrotic loci (A through I) can be distinguished. Immediately following contact between the retina and surface ectoderm (day 11) degenerating cells were observed in (A) the ventral extent of the optic vesicle, beginning i n the mid-retinal primordium and continuing ventrally i n the optic J. MORPH., 140. 159-170. 159
Gliicksmann ('51 ) observed that during normal mammalian ocular morphogenesis large numbers of cells become necrotic and are resorbed within the eye rudiment prior to and during invagination of the optic cup. Silver and Hughes ('73) observed that these resorptions are largely confined to the ventral aspect of the optic rudiment where the optic fissure subsequently forms. Evidence for the role of cell death during fissure formation and other morphe genetic events during eye development has remained unclear, however, since the quantity of degenerate cells cannot be selectively controlled in developing tissue by experimental means (Saunders, '66).Chase et al. ('41a) described a congenitally anophthalmic strain of mice in which, he proposed, retarded growth of the eye vesicle and the consequent failure of lens induction result in approximately 90% eyeless and 10% microphthalmic neonates. Upon reexamination of a sequence of embryos of the eyeless strain it was observed that during the earliest stages of ocular morphogenesis the regular sequence of necrotic loci, which Silver and Hughes ('73) have described in rat and other mammalian embryos, is entirely lacking.Our observations suggest that the first recognizable divergence between the morphology of timed mutant (strain zrdct-an) and control embryos (strain C57BL/6J) occurs during apposition of the optic vesicle and surface ectoderm but prior to the development of the retinal thickening and lens placode. In control embryos mesenchyme which becomes entrapped between the prospective retina and lens becomes necrotic and is resorbed. Conversely, in eyeless embryos the surfaces of the presumptive retina and lens, while closely apposed, are separated by variable numbers of mesenchymal cells which remain viable and can undergo mitoses throughout development. The failure of mesenchymal cells to degenerate may lead to the reduction in size of both retina and lens primordia. Contrary to Chase's ('41a) observations, in all anophthalmic embryos contact between the optic vesicle and lens epithelium is eventually established and a lens of variable size is induced. In most cases, however, the lens is displaced from the eye chamber by proliferation of the mesenchymal cell mass and the optic rudiment is subsequently resorbed. In the remaining embryos which presumably will become microphthalmic the lens reaches a critical dimension and is retained within the eye cup. In them, although cell death is absent from within the developing eye vesicle and cup, invagination can proceed as far as the retinal fissure stage. However, the optic fissure does not form. These observations suggest that there may be a relationship between morphogenetic cell death, formation of the optic fissure, and the production of severe congenital eye defects.One of the most complex patterns of normal mammalian ocular morphogenesis cellular death and resorption within a de-large numbers of cells become necrotic and veloping organ occurs during the early are resorbed within the retina and lens morphogenetic stages of...
U l t r a s t r u c t u r a l examination of s c i a t i c nerves from postnatal mice and r a t s revealed myelinated and nonmyelinated f i b e r s w i t h s t r u c t u r a l c h a r a c t e r i s t i c s s i m i l a r t o those seen i n Wallerian degeneration. Such f i b e r s a r e more commonly found between 7 and 14 days and a r e believed t o represent spontaneous axon degenerations during development.Recent q u a n t i t a t i v e s t u d i e s (Hughes and Egar, ' 7 2 ; P r e s t i g e and Uilson, ' 7 2 ) suggest decreases i n f i b e r number during c e r t a i n s t a g e s of amphibian peripheral nerve development. While i t has been suggested t h a t during maturation some of t h e nonmyelinated axons in mammalian peripheral nerves may undergo degeneration or resorption (Gamble and Breathnach, '65; Gamble, ' 6 6 ; Webster and C'Connell , '70) , evidence f o r such events has not been presented.axon degeneration can be observed in a maturing mammalian peripheral nerve.This study was t h e r e f o r e undertaken in order t o determine whether MATERIALS AND METHODS Mice used i n t h i s study were derived from an inbred CFWl colony maintained i n t h i s laboratory.Miller (Allison Park, Pa.) Sprague-Dawley r a t s were a l s o used.were housed i n a room maintained a t approximately 250 C and t h e n u r s i n g mothers were provided with Furina Lab Chow and t a p water ad l i b . After d e l i v e r y each l i t t e r was reduced t o s i x animals i n order t o insure t h a t a l l of the pups had equal access t o t h e mother's milk. All of t h e l i t t e r s from
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