We studied cerebral lesions in the streptozotocin-diabetic rat, an established model of diabetic retinopathy. A group of diabetic rats all had cerebral lesions, but showed no gross abnormalities of the brain or signs of effects on the central nervous system. Light and electron microscopy of horizontal brain sections stained by a variety of methods showed focal accumulation of collagen fibrils in the basement membranes of arteriole and capillary walls, slight degeneration of random neuronic cells (mainly in the brain stem), and no evidence of perivascular myelin pallor plaques. A marked tendency toward platelet aggregation, which leads to thrombosis, was also seen. There was no difference between results from rats killed 9 and 12 months after streptozotocin injection. The brain lesions bore a close resemblance to those seen in a nutritional encephalopathy known to be induced by a diet deficient in tocopherol and rich in oxidized oil, but differed from that encephalopathy in that the peculiar hypertrophic cerebral astroglia associated with diabetes resembled Alzheimer Type II astroglia. The differences between these cerebral astroglia and the retinal Müller cells may account for the difference in degree between the effects of diabetes on the brain and the retina.
Seventeen Wistar inbred rats were made diabetic by a single injection of streptozotocin (50 mg/kg body weight) and were killed after periods of 3, 6, 9 or 12 months. Pathological changes in pericapillary Müller cells of the retina were studied using electron microscopy. Basement membrane-like material proliferated in the intercellular space of the Müller cell network and occasionally appeared to insinuate into the Müller cell cytoplasm far from capillary pericytes and endothelial cells. The part of the Müller cell that was enveloped by proliferating basement membrane-like material showed partial necrosis which was thought to contribute to the widening of the capillary wall. A breakdown of the retinal framework, which leads to capillary dilatation, was also thought to be associated with partial necrosis of Müller cells. Highly electron-dense bodies accumulated in the Müller cell cytoplasm which surrounded the retinal capillaries. Ultrastructurally, these dense bodies resembled lysosomes. Their increased number might reflect the altered metabolism of the diabetic retina.
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