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The pigment epithelial cell of the retina actively participates in two aspects of lipid metabolism: (a) the fatty acid esterification of vitamin A and its storage and transport to the photoreceptors, and (b) the phagocytosis and degradation of the lipoprotein membrane disks shed from the photoreceptor cells. Study of the pigment epithelial cells of adult albino and pigmented rodents has revealed the abundance of an organelle, microperoxisomes, not previously known to exist in this cell type. The metabolism, transport, and storage of lipids are major functions of other cell types which possess large numbers of microperoxisomes associated with a highly developed smooth endoplasmic reticulum. Microperoxisomes were encountered, but relatively rarely, in Müller cells and vascular endothelial cells. A tubular system in photoreceptor terminals is reactive in the cytochemical procedure used to visualize microperoxisomes.

Glycine, when injected intravitreally, has an inhibitory action on the electroretinogram (ERG) of the rabbit resulting in a transient loss of the oscillatory potentials of the b-wave. This inhibitory action is reversible within 24 h after glycine injection. In autoradiographs, after [3H] glycine administration, the radioactive label is mainly found over the inner nuclear layer (INL) and inner plexiform layer (IPL) without predilection of specific cell types and/or synapses. Electron microscopy reveals cytopathological changes in amacrine cells, in particular their cell membranes. These changes are conspicuous especially 1-2 h after the injection and the cells become normal again within 24 h. It is concluded that glycine has an inhibitory action upon the rabbit ERG in vivo. This action, on the basis of our morphological observations under our experimental conditions, may be due to an overall somatic membrane action rather than to an action as inhibitory neurotransmitter at the synaptic level. The reversible cellular lesions of amacrine cells after glycine administration with a concomitant, transient loss of oscillatory potentials (OP) supports the hypothesis that the cellular origin of OP is situated in amacrine cells.

A large area of the posterior pole of the retina of the miniature pig was photocoagulated, and 2-3 wk later the PO2 in the preretinal vitreous was mapped with O2-sensitive microelectrodes. In the control retina, the PO2 was highly heterogeneous being much higher close to an artery than opposite an intervascular zone. After photocoagulation, PO2 opposite an intervascular zone was found to be significantly increased. A quantitative histologic analysis showed that in the photocoagulated areas more than 28% of the outer retina was destroyed. The authors conclude from these results that photocoagulation, by partially destroying the pigment epithelium-photoreceptor complex, causes an increase of the oxygenation of the retina.

The effects of laser-photo-coagulation on retina, pigment epithelium and choroid has been studied in animals (rabbit and mini-pig). During the first two hours after photocoagulation the permeability of the blood-retinal barrier and of the pigment epithelium is temporarily increased. Later on (2-4 days) pigment epithelial cells proliferate within the coagulated areas and "tighten" the epithelial leaks. Photoreceptor outer segments undergo during the same period reversible breakdown. Normal retinal blood vessels are hardly altered by photocoagulation whereas pathological or neoformed vessels may be obliterated. Functional deficiences are observed after extensive photocoagulations only and even then rarely implicated by the patients.

We describe histopathologic features of an enucleated eye of a patient suffering bilateral acute retinal necrosis (BARN). Retinal tissue was found focally degenerated, and the choroid massively enlarged by lymphoid-like agranular cells. An association of the disease with a viral infection could be demonstrated by (a) the presence of virus particles of the herpesvirus type in retinal tissue, (b) the transmission of the infected principle to human embryo fibroblast cultures, and (c) the visualization of CMV-antigens by immunofluorescence microscopy in such infected cultures. Slow growth of the virus in vitro and the presence of CMV-antigens after infection indicate that the herpesvirus involved in BARN was of the type CMV. On the basis of these findings we propose a guideline for therapy.