Format

Send to

Choose Destination
Exp Eye Res. 2002 May;74(5):615-25.

Early retinal damage in experimental diabetes: electroretinographical and morphological observations.

Author information

1
Bruce Rappaport Faculty of Medicine, Technion-Israel Institute of Technology and Rappaport Institute, Haifa, Israel.

Abstract

A growing body of evidence indicates that impairment of retinal function precedes the earliest signs of vascular complications. The aim of this study was to follow the development of retinopathy both functionally and morphologically in a rat model of diabetes mellitus. Diabetes was induced in rats by intravenous injection of streptozotocin (STZ). Age-matched rats raised under similar conditions served as control. The electroretinogram (ERG) was recorded in order to assess retinal function. The expression of glial fibrillary acidic protein (GFAP) in Müller cells was used as a cellular marker for retinal damage. The ERG responses of the diabetic rats were reduced in amplitude compared to the responses recorded from the control rats as early as 2 weeks after onset of diabetes. The b-wave was more affected than the a-wave. GFAP expression in the diabetic retina did not differ from that in the control retina during the first 5 weeks of diabetes. GFAP was demonstrated only in astrocytes in the vitreo-retinal border. After 6-7 weeks of diabetes, GFAP expression in the retinas of the diabetic rats was also detected in the endfeet of the Müller cells. With the progression of diabetes, GFAP expression spreads throughout the entire length of the Müller cells. In the retinas from control rats, GFAP expression was limited to astrocytes and was not detected in Müller cells even at 40 weeks of follow-up. The observations indicate that the functional integrity of retinal cells is compromised already at short time intervals after onset of experimental diabetes in rats.

PMID:
12076083
DOI:
10.1006/exer.2002.1170
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center