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Early monocular enucleations were done in rats, either at embryonic day 16 (E16) or on the day of birth, and the surviving uncrossed pathway was studied either at birth for some of the animals enucleated prenatally, or in the adult for all of the other animals. The uncrossed pathways were studied by using HRP as a retrograde tracer. The neonatal enucleations showed the increase of the surviving uncrossed component previously documented by others. In contrast to this, a prenatal enucleation produced a significant reduction in the surviving uncrossed pathway at birth. If these animals survived to be adults, then the surviving uncrossed pathway was slightly increased relative to normal. We conclude that two quite distinct mechanisms have been exposed by these experiments, one acting prenatally and producing a reduction in the uncrossed pathway, and the other acting postnatally and producing an increase. The postnatal effect, which is due to a decrease of the normally occurring ganglion cell death, thus neutralizes the prenatal effect, so that the most effective demonstration of the prenatal effect is to be seen before the period of cell death (early postnatal in rats and ferrets). The same methods were applied to prenatal ferrets at E26-E28 and, in order to see the maximum prenatal effects, the uncrossed pathways were studied at birth in all of these animals. There was a severe reduction of the uncrossed pathway throughout, and this was greatest in the animals with the earliest enucleations. Since the uncrossed pathway in normally reared albino animals is abnormally small, the effects of an early prenatal enucleation in albino rats and ferrets were compared with the effects in normally pigmented animals in order to determine whether the early enucleation was producing an abnormality comparable to the albino abnormality. Prenatal enucleations reduced the uncrossed pathway not only in normally pigmented but also in albino neonatal rats and ferrets. Further, the characteristic position of the nasal border of the temporal retina, which is abnormal in albino animals, was unaffected by the enucleation in either the albino or the pigmented animals, except where, in ferrets, enucleations produced a complete loss of the temporal concentration of ipsilaterally projecting ganglion cells (the temporal crescent). The earlier enucleations showed a greater tendency to produce such a complete loss of the temporal crescent. We conclude that the developmental mechanisms affected by the early enucleations are distinct from those that act to produce the albino abnormality even though both produce an abnormally small uncrossed pathway.(ABSTRACT TRUNCATED AT 400 WORDS)

An earlier study has shown that in young kittens, but not in adult cats, section of one optic nerve produces a curious pattern of cell survival in the denervated geniculate laminae. Most of the cells in these laminae are shrunken, but a few large cells remain close to the borders of the adjacent, normally innervated laminae, giving the impression that these cells are sustained by collaterals arising &om the normal retinogeniculate axons.Adult cats and kittens aged 7, 9 and 20 days have been used to determine the extent to which normal retinogeniculate axons can invade a denervated genicd a t e lamina. One eye was removed and the animals were kept for periods varying from four months to four years. The fiber degeneration produced by removal of the second eye was then studied. There is no evidence for any collateral sprouting in the adults. If the first operation is done at seven or nine days a limited number of axons grow across laminar borders and invade a small border zone of the denervated laminae. These axons do not appear in all of the regions that show surviving large border cells.It is concluded that new sprouts are probably not formed, but that growing axons can invade an inappropriate lamina if this is denervated during the normal period of axonal growth.

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