Morphological and morphometric study of peripheral nerves from rats with streptozotocin-induced diabetes mellitus

Abstract

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.

The effects of Sorbinil on peripheral nerve conduction velocity, polyol concentrations and morphology in the streptozotocin-diabetic rat

“…Axon area remained at onset levels, as did conduction velocity in untreated diabetic rats, whereas normal animals showed age-related increases in both these parameters. The retardation in axon growth is in agreement with other light and electron microscopy studies [4,13,19] using relatively mature rats, although Zemp et al [20] found that axons grew normally when diabetes was induced in very immature animals. The reason for such age-related differences is not known and requires further investigation, but paradoxically it appears that diabetes during the rapid growth phase has less effect on axons than when they are more fully developed.…”

Rosuvastatin positively changes nerve electrophysiology in diabetic rats

“…Those rats are characterized by high hyperglycaemia and markedly increased axonal and myelin thickness impairment, whereas in our model hyperglycaemia is more moderate and this makes it possible to test treatments over several months. In addition, in our model, nerve conduction velocities became markedly reduced only after 6 months of diabetes, due to the protection of neural growth during maturation [20,21]. This was shown using the same model in which we previously reported a trend towards an improvement in peripheral nerve conduction after short-term treatment with cerivastatin [15].…”

“…However, the fact that significant correlations between sensory parameters seen in normal rats during maturation (3-4 months) are not found in diabetic rats indicates early electrophysiological changes, at least for sensory nerve function, in diabetes. Nerve conduction velocities are markedly reduced only later, at 6 months, in agreement with the protection of neural growth during maturation [20,21].…”

Diabete Como Modelo De Neuropatia Autonômica

“…Entretanto, as doses efetivas ou letais do aloxane ou da STZ variam consideravelmente entre as espécies e são altamente sensíveis à idade, sexo e estado nutricional dos animais 21 . Uma injeção única, intraperitoneal ou intravenosa de aloxane ou STZ, preferencialmente com os animais em jejum, induz diabete experimental em ratos que pode ser mantido sem tratamento com insulina por um ou dois anos 3,22,23 . Em geral, STZ é mais eficaz e mais específica para as células beta do pâncreas que o aloxane 12 .…”