DISRUPTION OF THE RETINAL BASAL LAMINA DURING EARLY EMBRYONIC-DEVELOPMENT LEADS TO A RETRACTION OF VITREAL END FEET, AN INCREASED NUMBER OFGANGLION-CELLS, AND ABERRANT AXONAL OUTGROWTH

Bacterial collagenase was injected into the vitreous of the eye of chi ck and quail embryos. Immunocytochemical and ultrastructural studies r evealed that the collagenase dissolved the retinal basal lamina of the injected eye. The basal lamina disruption was first detectable 1 hour after enzyme injection and was complete within 3 hours. With further development, the retinal basal lamina was not reestablished; newly dev eloping neuroepithelium in the peripheral retina, however, generated a n intact basal lamina. Western blot analysis showed that Clostridial c ollagenase degraded various collagens but spared noncollagenous protei ns. Basal lamina disruption of embryonic day 3 to 6 retinae led to the retraction of the end feet of the neuroepithelial cells, caused an in crease in the number of Islet-1(+) cells (most likely ganglion cells), an increase in the thickness of the optic fiber layer, and aberrant g rowth of optic axons on their way toward the optic disc. None of these changes were observed when retinal basal laminae were disrupted at la ter stages of development. The present data demonstrate that the retin al basal lamina, by anchoring the neuroepithelial cells to the pial su rface of the retina, has an important function in the development of t he normal cytoarchitecture of this structure. It is proposed that the altered extracellular environment in the vitreal part of the retina, r esulting in the retraction of the neuroepithelial end feet, is respons ible for the increased number of Islet-1(+) cells and the aberrant axo nal navigation. (C) 1998 Wiley-Liss, Inc.