Early reaction of astroglial cells in rat hippocampus to streptozotocin-induced diabetes

Diabetic patients show impaired brain functions, although underlying mechanisms remain unclear. Little is known as well about early diabetes-related changes in a brain tissue. To investigate them we analyzed the reaction of astroglial cells in the hippocampus of rats rendered diabetic by a single in...

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Veröffentlicht in:Neuroscience letters 2008-10, Vol.444 (2), p.181-185
Hauptverfasser: Lebed, Yurii V., Orlovsky, Maxim A., Nikonenko, Alexander G., Ushakova, Galina A., Skibo, Galina G.
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Sprache:eng
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Zusammenfassung:Diabetic patients show impaired brain functions, although underlying mechanisms remain unclear. Little is known as well about early diabetes-related changes in a brain tissue. To investigate them we analyzed the reaction of astroglial cells in the hippocampus of rats rendered diabetic by a single injection of streptozotocin (STZ). Astrocyte count, size and shape as well as levels of glial fibrillary acidic protein (GFAP) and S100b protein were assessed 3, 7 and 14 days after the STZ injection using immunohistochemistry, immuno-enzyme assay and computer-assisted image analysis. The reduced GFAP-positive cell count was found on day 3 when these cells were significantly smaller and less arborized with respect to the control. This tendency reversed on day 7 when more numerous GFAP-positive cells grew in size and became more ramified. S100b-positive cell count changes followed a contrasting pattern, elevating on days 3 and 7 and dropping on day 14. The level of cytoskeletal GFAP changed in parallel with GFAP expression revealed by immunocytochemistry, while cytosolic GFAP level started to increase only 7 days after the STZ injection. At the same time S100b level experienced an elevation on day 3 reaching the peak on day 7 and decreasing afterwards. These results suggest that the reaction of astroglial cells may be the earliest response of the brain tissue to an altered glucose metabolism playing presumably the critical role in the mechanisms underlying diabetes-related impairments of brain functions.
ISSN:0304-3940
1872-7972
DOI:10.1016/j.neulet.2008.07.094