Early electroretinographic features of streptozotocin-induced diabetic retinopathy
Article first published online: 18 DEC 2007
Clinical & Experimental Ophthalmology
Volume 35, Issue 9, pages 847–854, December 2007
How to Cite
Shinoda, K., Rejdak, R., Schuettauf, F., Blatsios, G., Völker, M., Tanimoto, N., Olcay, T., Gekeler, F., Lehaci, C., Naskar, R., Zagorski, Z. and Zrenner, E. (2007), Early electroretinographic features of streptozotocin-induced diabetic retinopathy. Clinical & Experimental Ophthalmology, 35: 847–854. doi: 10.1111/j.1442-9071.2007.01607.x
- Issue published online: 18 DEC 2007
- Article first published online: 18 DEC 2007
- Received 27 May 2007; accepted 27 August 2007.
- diabetic retinopathy;
Background: This study set out to document the early electrophysiological and immunohistochemical changes that occur in the retina of experimentally induced diabetic rats.
Methods: Diabetes was induced in rats by intraperitoneal injection of 60 mg/kg of streptozotocin (STZ). Electroretinogram readings were taken monthly under either short-duration or long-duration stimuli for up to 3 months after STZ. Oscillatory potentials (OP) and the amplitudes and implicit times of a- and b-waves were analysed, and b-wave amplitudes were analysed using a Naka–Rushton fit. Scotopic a-waves were analysed with photoreceptor models, and Rmp3 (the maximum a-wave amplitude) and S (sensitivity) were calculated. Three months after STZ injection, immunohistochemistry for glial fibrillary acidic protein was performed on the retinas of the STZ-treated rats and age-matched controls.
Results: The implicit OP times were significantly longer in the diabetic rats as compared with the controls, and this difference was noted as early as 1 month following STZ treatment. Other electrophysiological parameters, such as OP amplitudes, a- and b-wave amplitude as well as the implicit times, did not differ from controls at this stage. The sacrificed STZ-treated rats also demonstrated marked enhancement of glial fibrillary acidic protein immunoreactivity, suggesting that at least in experimentally induced diabetic retinopathy there is increased Müller cell reactivity.
Conclusion: The results of this study indicated that functional alterations in the retina develop rapidly after the onset of diabetes. Analysis of each electroretinogram component may be useful in further investigating the development mechanisms of diabetic retinopathy.