Eight streptozotocin-injected Wistar rats and eight controls were fixed by whole-body perfusion 4 months after beginning of the experiment, the nervus radialis was dissected and processed for light and electron microscopy. After light-microscopic study standard photographs of nerve cross sections were measured by means of a semiautomatic image analyzer. The following measurements were obtained: (1) surface of fibers, axons, and myelin sheaths, (2) ratio of myelin to axon surface, and (3) percent of endoneural space. Group means and standard deviations were calculated, and cumulated size class distributions were made. Representative nerve specimens from all animals were also studied by electron microscopy. The quantitative study revealed in the diabetics a severe reduction of the average myelin surface, a mild increase of axonal cross section and of endoneural space, a reduction of myelin/axon ratio and a mild reduction in cross section of the nerve. Ultrastructural lesions of minor degree were found in the cytoplasm of Schwann and mesenchymal cells, no lesion was observed in axons. These findings demonstrate the presence of neuropathy 4 months after induction of diabetes and support the pathogenetic role of the Schwann cell in our experimental model.
One year after beginning of the experiment seven streptozotocin-injected Wistar rats and seven controls were fixed by whole-body perfusion, the nervus radialis was dissected and processed for light and electron microscopy. After light-microscopic study standard photographs of nerve cross sections were measured by means of a semiautomatic image analyzer. The following measurements were obtained: (1) surface of fibers, axons, and myelin sheaths; (2) ratio of myelin to axon surface; and (3) percent of endoneural space. Group means and standard errors were calculated, and cumulated class distributions were made. Ultrathin sections from all animals considered morphometrically were studied qualitatively for ultrastructural changes. The quantitative study revealed in the diabetics reduction of average myelin surface, increase of endoneural space, and reduction of myelin/axon ratio. The main ultrastructural findings were lesions of Schwann and mesenchymal cells, followed by less frequent and less severe changes in axons and endothelium. These results suggest a primary Schwann cell lesion was responsible for the observed myelin reduction.
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