Morphologic studies of the retina in a new diabetic model; SHR/N:Mcc-cp rat

The pathogenesis of diabetic retinopathy has not been fully explained. The earliest histological lesion is the loss of intramural pericytes and thickening of the basement membrane. Increased activity of the polyol pathway is a probable mechanism for these two abnormalities. Investigations have suffered from the lack of an exact animal model simulating the human condition. Examination of the retina in the spontaneously diabetic SHR/N:Mcc-cp rat demonstrated degeneration and loss of intramural pericytes, a progressive increase in basement membrane thickness, and microinfarctions with an area of non-perfusion. Therefore, this model may be used to clarify the biochemical mechanisms linking the metabolic abnormalities of diabetes and retinopathy.

Freeze-fracture Scanning Electron Microscopy of the Human Retina

Our current understanding of the ultrastructure of the retina has been gained using transmis sion electron microscopy (TEM) of thin sections. Scanning electron microscopy was proven to be a very valuable adjunct to TEM in retinal research. The present study describes the surface features of the retina. The complex shape of Muller cells varies in different layers of the retina. The Muller cell processes surround the cell bodies in the ganglion cell Iayer and form a part of the inner limiting membrane. The external limiting membrane consists of tight junctions between the beginning of the photo receptors and the Muller cells. The Muller cells extend beyond the external limiting membrane to embrace the photoreceptors. The course of the fibers of the outer plexiform layer is almost parallel to the surface of the macula. The interphotoreceptor space has a reticular structure.