Abstract
P 090
Assessment of long-term changes in retinal vasculature in the InsAkita diabetic mouse using two-photon microscopy
Frank Schlichtenbrede1, Franziska vom Hagen2, Florian Rensch1, Frederick Pfister2, Thomas Euler3, Jost B. Jonas1
1Universitäts-Augenklinik, Klinikum Mannheim, Universität Heidelberg, Mannheim, 2Innere Medizin V, Klinikum Mannheim, Universität Heidelberg, Mannheim, 3Biomedizinische Optik, Max Plank Institut für Medizinische Forschung, Heidelberg
Objective
Diabetes causes neuronal degeneration and vascular damage in the human retina. Here we assess long-term changes of retinal morphology in the diabetic mouse model using 2 Photon microscopy.
Methods
Whole-mounted retinal explants of wildtype mice and mice (6 months after onset of diabetes) were life-stained with and then analyzed morphologically using two-photon microscopy. Three independent observers analyzed changes in layer thickness and retinal vasculature, as well as tissue integrity and cell viability. For the latter we made use of the fact that in the retina SR101 stains the somata of damaged neurons but not healthy ones.
Results
Overall retinal morphology was intact in all animals. Retinal thickness was significantly reduced in diabetic mice as compared to wild type mice, predominantly in the inner retinal layers. Qualitatively, vascular occlusions and acellular capillaries were found in the intermediate and deep vascular layers of diabetic mice, but not in the superficial vascular layer. In wildtype mice, these abnormalities were not observed. After 6 months of diabetes, we could not observe an increase in SR101-positive, suggesting that neurons are not substantially damaged.
Conclusions
We demonstrate a detailled analysis of retinal architecture in mice with longstading diabetes. While diminished layer thickness mainly in the inner (vascularized) layer suggest a vascular degeneration resulting in capillary occlusion, no increase in damaged cells was seen at this stage. Further studies shall clarify the time course of neuroglial degeneration and the relation to microangiopathy in this prototype model.
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