Pyramidal neurons within the cerebral cortex are known to make long-range horizontal connections via an extensive axonal collateral system. The synaptic characteristics and specificities of these connections were studied at the ultrastructural level. Two superficial layer pyramidal cells in the primate striate cortex were labeled by intracellular injections with horseradish peroxidase (HRP) and their axon terminals were subsequently examined with the technique of electron microscopic (EM) serial reconstruction. At the light microscopic level both cells showed the characteristic pattern of widespread, clustered axon collaterals. We examined collateral clusters located near the dendritic field (proximal) and approximately 0.5 mm away (distal). The synapses were of the asymmetric/round vesicle variety (type I), and were therefore presumably excitatory. Three-quarters of the postsynaptic targets were the dendritic spines of other pyramidal cells. A few of the axodendritic synapses were with the shafts of pyramidal cells, bringing the proportion of pyramidal cell targets to 80%. The remaining labeled endings were made with the dendritic shafts of smooth stellate cells, which are presumed to be (GABA)ergic inhibitory cells. On the basis of serial reconstruction of a few of these cells and their dendrites, a likely candidate for one target inhibitory cell is the small-medium basket cell. Taken together, this pattern of outputs suggests a mixture of postsynaptic effects mediated by consequence the horizontal connections may well be the substrate for the variety of influences observed between the receptive field center and its surround.

Macaque monkeys become myopic when raised with fused lids to expose the retina to formless shadows during the period of postnatal eye development. The effect of the abnormal visual input is an excessive expansion of the posterior segment of the eye, a process that seems to be controlled by the nervous system. The mechanism by which the nervous system influences eye growth appears to be different in the stumptailed macaque (Macaca arctoides) and the rhesus macaque (M. mulatta). Lid-fused arctoides monkeys do not develop myopia when the ciliary muscle is paralysed or the optic nerve is cut, suggesting that the abnormal growth is caused by excessive accommodation. In contrast, paralysis of the ciliary muscle or optic nerve section does not prevent the development of myopia in the rhesus macaque, suggesting that in this species the axial growth is controlled by the retina. In both species neonatal lid fusion causes a marked increase in retinal vasoactive intestinal polypeptide (VIP). VIP is contained in a single type of amacrine cell whose dendrites spread in the middle of the inner plexiform layer. It remains to be determined whether the increase in the level of VIP is related to the abnormal axial elongation caused by lid fusion. At present we are also exploring the effects of accommodation on the growth of the eye by training juvenile arctoides monkeys to work on complex visual discrimination paradigms. Preliminary results show that performing a visual task at close range may influence the axial length and refraction in this macaque species.

The binding of RPE‐1, a mouse monoclonal antibody selective for newt retinal pigment epithelium, was followed in eyes undergoing embryonic developemnt and retinal regeneration. Using the indirect immunofluorescence technique on frozen sections, we observed bright and continuous labelling exclusively in the retinal pigment epithelium (RPE) of normal adult newts, but labelling became diminished near the ora serrata region and stopped abruptly at the ciliary margin. During development, labelling was not detected in the retinal pigment epithelium (RPE) until the formation of photoreceptor outer segments and was not observed in any other ocular tissue. There was no correlation between the appearance of pigment in retinal pigment epithelial cells and their labelling with the RPE‐1 antibody. Furthermore, albino salamander embryos showed the same pattern of labelling with RPE‐1 as that seen in age‐matched pigmented animals. During retinal regeneration, RPE cells were labelled less intensely, but heavy labelling was observed in the newly formed retinal cells. With time, labelling in regenerated retina receded, so that by the end of regeneration, labelling by RPE‐1 was once more restricted to the RPE cells. The identification of RPE‐1 as a marker for postmitotic retinal neurons about to undergo differentiation provides a promising approach for further studies of regeneration with the help of molecular tools.

Lids were fused in six neonatal and one adult macaque monkey (Macaca mulatta and Macaca arctoides) and were kept fused for 1 to 18.5 months. The juvenile macaques, but not the adult one, developed myopia due to excessive elongation of the eye. In all animals, the immunohistochemical reactivity of the retina for vasoactive intestinal polypeptide (VIP) was much higher in the closed than in the open eyes. The neuropeptide was localized to the perikaryon and dendrites of amacrine cells. No difference was observed in substance P immunoreactivity between open and closed eyes, suggesting that the observed effect is selective. The change in VIP immunoreactivity could be the result of an increase in peptide synthesis, a decrease in peptide release, or a combination of the two. These results indicate that VIP may play a part in the regulation of postnatal ocular growth.

Acta OphthalmologicaVolume 66, Issue S185 p. 91-92 The mechanism of lid-suture myopia Elio Raviola MD, Corresponding Author Elio Raviola MD Boston & New York, USAProfessor of Anatomy and Cellular Biology, 25 Shattuck Street, Boston, MA 02115–6092, USA.Search for more papers by this authorTorsten N. Wiesel, Torsten N. Wiesel Boston & New York, USASearch for more papers by this author Elio Raviola MD, Corresponding Author Elio Raviola MD Boston & New York, USAProfessor of Anatomy and Cellular Biology, 25 Shattuck Street, Boston, MA 02115–6092, USA.Search for more papers by this authorTorsten N. Wiesel, Torsten N. Wiesel Boston & New York, USASearch for more papers by this author First published: April 1988 https://doi.org/10.1111/j.1755-3768.1988.tb02675.xCitations: 1AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article.Citing Literature Volume66, IssueS185April 1988Pages 91-92 RelatedInformation

Myopia develops in macaque monkeys when their lids are surgically fused at birth and kept closed for one year. This experimental refractive error has many features in common with human myopia: It is caused by progressive axial elongation of the eye, is often accompanied by fundus changes, and can only be induced before eye growth has been completed. Myopia does not develop in animals raised in the dark; thus, it is triggered by an alteration of the visual input and is presumably mediated by the nervous system. In Macaca arctoides, atropine administration prevents abnormal eye elongation, and this suggests that lid-fusion myopia is caused by excessive accommodation. In M. mulatta, atropine is ineffective; furthermore, myopia develops when lids are sutured after interruption of the optic pathways. Thus, in this species accommodation can be ruled out as a determinant of eye elongation, and other neural mechanisms may be responsible for the refractive error. Our experiments suggest that the refractive state is largely programmed on a genetic basis, but that an abnormal visual experience can disrupt the process of postnatal eye growth and induce axial myopia.

The cornea of one eye was opacified in two young macaque monkeys by multiple stromal injections of a suspension of polystyrene particles (latex). Ultrasound measurements showed that the eye with opaque cornea grew at a faster rate, so that after 1 year it was more than 1 mm longer than the normal eye. This difference in axial length was due to elongation of the posterior segment, since lens thickness, depth of anterior chamber, and corneal curvature were identical in both eyes. At histological examination, no pathological changes were observed in the anterior segment of the latex-injected eye except for a scant vascularization of the corneal opacity. The result of this experiment demonstrates that opacification of the corneal has effects on axial length similar to, although less marked than, those on lid fusion and therefore supports our previous conclusion that the myopia caused by lid fusion is triggered by the abnormal visual impact and involves central visual pathways.