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Invest Ophthalmol Vis Sci. 2006 Nov;47(11):5116-24.

An electrophysiological study of retinal function in the diabetic female rat.

Author information

1
Departments of Ophthalmology and Visual Sciences, University of Illinois at Chicago, College of Medicine, 1955 W. Taylor Street, Chicago, IL 60612, USA. dramse1@uic.edu

Abstract

PURPOSE:

To examine retinal function in female Long-Evans rats with streptozotocin (STZ)-induced diabetes.

METHODS:

Hyperglycemia was induced by IV injection of STZ, and ERG responses were recorded at 4-week intervals over 12 weeks. Oscillatory potentials (OPs) and responses to intermittent stimulation were analyzed with a custom computer program. The GABA-induced responses of individual rod bipolar cells were obtained from patch-clamp recordings, and immunohistochemistry was used to illustrate the retinal distribution of GABA (gamma-aminobutyric acid) and GABA(C) receptors.

RESULTS:

Hyperglycemia developed in rats 2 to 3 days after injection of STZ. Compared with previous reports of the effects of diabetes in male rats, visual function abnormalities appeared to be milder in STZ-treated female rats. No significant differences were observed in the sensitivity or amplitude of the a- or b-wave components of the ERG between diabetic and control animals, and both animal groups exhibited a similar time course of neuronal dark adaptation. In contrast, diabetic animals showed significant differences in the pattern of OPs and in the amplitudes of their responses to flicker. The accumulation of GABA in the inner retina of diabetic rats, combined with the results of patch-clamp recordings from individual bipolar cells, revealed that the circuitry underlying the GABA signal of the proximal retina is affected by hyperglycemia.

CONCLUSIONS:

The results suggest that changes in the GABA-signaling pathway may be the underlying cellular mechanism for altered ERG responses in STZ-induced diabetes in rats. Recognition of these early neurosensory defects would enable a better understanding of the pathophysiological basis of diabetic retinopathy.

PMID:
17065533
DOI:
10.1167/iovs.06-0364
[Indexed for MEDLINE]

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