Abstract

Purpose:This study analyzes the structures of optic nerve elements, i.e., glial cells and nerve fibers, in an STZ-induced hyperglycemic animal model. Morphological changes in glial elements of the optic nerve in hyperglycemic and normoglycemic animals were compared.Methods:Transmission electron microscopy, histochemistry, immunohistochemistry, and morphometry were used in this study.Results:Hyperglycemia increased the numbers of inner mesaxons and axons with degenerative profiles. Furthermore, it led to both an increase in the amount of debris and in the numbers of secondary lysosomic vesicles in glial cytoplasm. Hyperglycemia also led to a decrease in glial fibrillary acidic protein expression and an increase in periodic acid-Schiff-positive deposits in the optic nerves of hyperglycemic animals.Conclusion:We conclude that the damage to the structural elements observed in our animal models contributes to the pathogenesis of optic neuropathy in the early stages of diabetes.

Highlights

  • Diabetic ophthalmopathy is one of the most common chronic complications of diabetes mellitus, and includes ocular pathologies such as cataract, glaucoma,[1,2] diabetic retinopathy, and optic neuropathy.[2]

  • We describe the structural characteristics of glial cells in the optic nerves

  • STZ‐induced hyperglycemia has been shown to be a reliable experimental model to study the effects of hyperglycemia in the optic pathway

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Summary

Introduction

Diabetic ophthalmopathy is one of the most common chronic complications of diabetes mellitus, and includes ocular pathologies such as cataract, glaucoma,[1,2] diabetic retinopathy, and optic neuropathy.[2]. Cellular and molecular studies in retinas of hyperglycemic experimental animals suggest that neurons are vulnerable to hyperglycemia and are damaged shortly after the onset of the disease before any signs of vascular damage.[3,4] Diabetic optic neuropathy is a clinical condition involving the optic pathway. It may be asymptomatic and can only be detected using electrophysiological measurements.[5] This pathology, which has not been deeply studied, might develop in the absence of diabetic retinopathy. We describe the structural characteristics of glial cells in the optic nerves

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