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The rostral thalamo-hyperstriatal projection in young chicks was examined following large injections of wheat germ agglutin labelled with horseradish peroxidase (HRP-WGA) into the hyperstriatum. Retrograde labelling of thalamic neurons was present in the dorsolateral thalamus, rostrolateral part (DLAlr) and dorsolateral thalamus, lateral part (DLL). There was no evidence of a contralateral projection from the lateral anterior thalamic nucleus (LA) to the posterior aspect of the visual hyperstriatum as reported recently by Boxer and Stanford (1985). Furthermore, a comparison of labelled neurons in the contralateral rostral thalamus following injections into either the left or right hyperstriatum revealed no difference in the number of neurons. The study could therefore not confirm the presence of an asymmetrical LA-hyperstriatal projection, as reported by the above authors.

The visual projections of the remaining eye of posthatch congenitally monophthalmic chicks were examined using wheat germ agglutinin-horseradish peroxidase. The morphology of the primary visual centres and their retinal projections contralateral to the injected eye were similar to those of normal chicks. The ipsilateral primary visual centres were smaller and less organized, yet all received retinal input. These ipsilateral retinal projections differ from those found in normal posthatch chicks [O'Leary et al.: Devl. Brain Res. 10: 93–109, 1983] in that they are more extensive and occupy some centres not previously reported to receive input. In the case of the ipsilateral isthmo-optic projection to the retina there was a substantial increase in the number of cells compared with normal chicks [O'Leary and Cowan: Devl. Brain Res. 12: 293–310, 1984]. A comparison of the extent of ipsilateral retinal afferents with that of normal chicks suggests that following loss of an eye two responses occur within the visual centres: in some centres there is a massive increase in the amount of ipsilateral terminals, whereas in others there is only a small increase. We propose that these responses are related to the intrinsic retinotopy within the visual centres. That is, highly retinotopic visual centres do not normally contain ipsilateral fibres, but following eye removal fibres from the ipsilateral eye are able to substantially innervate these regions. Presumably this effect is due to loss of the overriding influence of contralateral input, which would normally recognize and eliminate inappropriate ipsilateral fibres. In poorly retinotopic regions ipsilateral fibres are able to persist in both normal and monophthalmic chicks, as recognition cues may not be as precise as in highly retinotopic regions. Thus, the greater the retinotopic precision, the finer the cues able to recognize ipsilateral fibres.

This study examines the morphology of sporadic congenital microphthalmia in 1-day-old chicks, with particular emphasis on the neural retina. On the basis of the size of the eyeball it is possible to classify microphthalmia into two groups, severe and mild. In severe microphthalmia (less than 5 mm in equatorial diameter), the eyeball is severely malformed, but in most cases it shows evidence of an organized neural retina. Although ganglion cells and an optic nerve head are present in a small proportion of these retinae, we could not trace an optic nerve projection to the brain. These results indicate that some ganglion cells are able to be sustained after the period of naturally occurring cell death, suggesting either that those ganglion cells have established some contact with the central nervous system or that the presence of their axons in a rudimentary optic nerve is adequate for survival. In mild microphthalmia (greater than 5 mm in equatorial diameter), the most consistent abnormality is a defect in the pecten, which together with other abnormalities such as orbital cysts and colobomas indicates that the major abnormality occurs in the region of the choroid fissure. Associated with these defects are abnormalities within the ganglion cell layer. In some cases the number of ganglion cells was reduced, and in others the numbers of both ganglion and displaced amacrine cells were reduced. Unexpectedly, there were localized regions completely devoid of cells in the ganglion cell layer. The timing of the congenital defect may provide some clue as to the presence of a critical period in which displaced amacrine cells are formed or are sensitive to events related to ganglion cell loss.

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