Abstract
Schwann cell disturbance followed by segmental demyelination in the peripheral nervous system occurs in diabetic patients. Since Schwann cell and oligodendrocyte remyelination in the central nervous system is a well-known event in the ethidium bromide (EB) demyelinating model, the aim of this investigation was to determine the behavior of both cell types after local EB injection into the brainstem of streptozotocin diabetic rats. Adult male Wistar rats received a single intravenous injection of streptozotocin (50 mg/kg) and were submitted 10 days later to a single injection of 10 microL 0.1% (w/v) EB or 0.9% saline solution into the cisterna pontis. Ten microliters of 0.1% EB was also injected into non-diabetic rats. The animals were anesthetized and perfused through the heart 7 to 31 days after EB or saline injection and brainstem sections were collected and processed for light and transmission electron microscopy. The final balance of myelin repair in diabetic and non-diabetic rats at 31 days was compared using a semi-quantitative method. Diabetic rats presented delayed macrophage activity and lesser remyelination compared to non-diabetic rats. Although oligodendrocytes were the major remyelinating cells in the brainstem, Schwann cells invaded EB-induced lesions, first appearing at 11 days in non-diabetic rats and by 15 days in diabetic rats. Results indicate that short-term streptozotocin-induced diabetes hindered both oligodendrocyte and Schwann cell remyelination (mean remyelination scores of 2.57 +/- 0.77 for oligodendrocytes and 0.67 +/- 0.5 for Schwann cells) compared to non-diabetic rats (3.27 +/- 0.85 and 1.38 +/- 0.81, respectively).
Highlights
Segmental demyelination is a prominent feature of the symmetric polyneuropathy of diabetic patients [1,2], probably due to Schwann cell disturbance
Since Schwann cell and oligodendrocyte remyelination in the central nervous system is a well-known event in the ethidium bromide (EB) demyelinating model, the aim of this investigation was to determine the behavior of both cell types after local EB injection into the brainstem of streptozotocin diabetic rats
Since Schwann cell and oligodendrocyte remyelination in the central nervous system (CNS) is a well-known event in demyelinating diseases such as multiple sclerosis [15,16,17] as well as in the EB gliotoxic model, the aim of the present investigation was to determine the behavior of these myelin-repairing cells after local EB injection in the brainstem of rats submitted to the diabetogenic model of streptozotocin
Summary
Segmental demyelination is a prominent feature of the symmetric polyneuropathy of diabetic patients [1,2], probably due to Schwann cell disturbance. Oligodendroglial damage induced by EB produces primary demyelinating lesions at the site of injection, with subsequent remyelination performed by surviving oligodendrocytes and by invasive Schwann cells [4,5,6,9,12,13,14]. Since Schwann cell and oligodendrocyte remyelination in the CNS is a well-known event in demyelinating diseases such as multiple sclerosis [15,16,17] as well as in the EB gliotoxic model, the aim of the present investigation was to determine the behavior of these myelin-repairing cells after local EB injection in the brainstem of rats submitted to the diabetogenic model of streptozotocin
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