| Abstract: | Chick embryos and young hatchling chicks have undergone unilateral retinal ablation and the brains were subsequently prepared for modified Fink-Heimer staining to detect degenerating axoplasm. Additional animals have been injected with tritiated proline or combinations of tritiated proline and tritiated fucose. In examining the patterns of degeneration and labelling produced, it appears that during the stage 40–44 period of embryonic life there is a critical period during which damage to retinal axons produces degeneration not only in the direct targets of the optic tract (primary centers), but also in a number of nuclei not projected to by the optic tract (secondary centers). By examining various survival times following retinal ablation and animals of varying embryonic and post-hatch age, we have concluded that retinal ablation during the critical period causes a rapid and fulminant degeneration in the secondary centers because they are all targets of the projection from the optic tectum, itself a prime target of the optic projection. Presumably, interruption of the retino-tectal projection during the critical period disrupts some as yet undefined trophic relationship between these two sets of neurons. Our studies show that the observed degenerative reaction in the secondary centers occurs most strongly in chick embryos between stage 40 and stage 44. This period coincides with the onset of synaptogenesis in the retino-tectal system (Rager, '76a,b). We therefore hypothesize that during this period some property or influence is passing from the retinal to the tectal neurons such that interruption of this process leads to death of the tectal neurons. |
