Utilizing adult albino rats and lanthanum nitrate as a tracer, electron microscopic studies were done to provide additional information on the blood-optic nerve barrier. Following injection into the cervical artery, lanthanum was observed to fill the intercellular space of the optic nerve parenchyma. Diffusion from the prelaminar optic nerve into the juxta-optic nerve retina was, however, prevented by the Kuhnt tissue at the level of the rod and cone layer. In this region, tight junctions were found between the glial cells of the Kuhnt intermediary tissue and were continuous from the tight junctions of the retinal pigment epithelial cells to the junctions (zonulae adhaerentes) of the outer limiting membrane. From the level of the outer limiting membrane to the inner limiting membrane there was no diffusion of lanthanum into the adjacent retina despite the absence of tight junctions, and the lanthanum which had diffused from the choroid was never observed in the area of the inner limiting membrane of the optic nerve head. It is in this region that the functional barrier may exist.
Chloroquine retinopathy was produced experimentally in the eye of the albino corydoras (one of the tropical fish) by daily administration of chloroquine (0.1 mg per os). The enucleated eyes were examined from the 14th day to 3 months after the beginning of drug administration under light and electron microscopy. The first change of retina was the appearance of membraneous cytoplasmic body (MCB) in the cytoplasm of ganglion, amacrine, bipolar and horizontal cells. MCB might be degenerated lysosome. They showed lamellar figures or crystalline lattice-like structures. Secondarily, these MCB appeared in the inner segments of photoreceptor cells. The outer segments of rod cells disappeared, and then those of cone cells. Although photoreceptor cells were diminished in number in advanced degeneration, the cells of inner nuclear layer and ganglion cells were maintained in number. The presence of MCB dose not mean death of cells. The retinal pigment epithelial cells contained MCB in its cytoplasm only in severe degenerative cases, and did not show other remarkable changes. MCB also appeared in the cytoplasm of perictyes of retinal vessels. Chloroquine is considered to damage directly photoreceptor cells most severely.
The photoreceptor cell endings of goldfish retinas were examined using ultrathin and freeze-fracture techniques. The synaptic vesicles could be seen lying closely packed in rows on each side of the synaptic ribbon, and the vesicles nearest to the end of the ribbon could be seen to be in direct contact with the presynaptic membrane. The openings of the synaptic vesicles to the synaptic cleft could also be observed at the presynaptic membrane nearest to the end of the ribbon, that is, 100 nm distant from the center of the apex. In the freeze-fractured replicas of the presynaptic membrane, the band-shaped membrane particle aggregation was seen at the apex and a row of the crater-like or circular protuberances were observed at each side of the apex. These structures were considered to be changes of the presynaptic membrane organizations according to the synaptic vesicle exocytosis. It may be possible that the synaptic vesicle exocytosis in the photoreceptor cells occurs at the sites of the presynaptic membrane nearest to the apical end of the synaptic ribbon, and that the exocytotic sites form a line on each side of the apex.
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