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M. K. Kim, D. E. Olson, P. M. Thule, N. Pozdeyev, P. M. Iuvone, M. T. Pardue; Low Intensity Stimuli of Scotopic Electroretinography Reveals Neuronal Changes in the Inner Retina of the STZ-Induced Diabetic Mice. Invest. Ophthalmol. Vis. Sci. 2009;50(13):5902.
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© ARVO (1962-2015); The Authors (2016-present)
While diabetic retinopathy (DR) is clinically diagnosed due to vascular changes, increasing numbers of studies suggest retinal dysfunction preceding vasculature changes. Our focus is to non-invasively detect abnormalities in DR using scotopic electroretinography (ERG). Previously, we reported the sensitivity of low intensity stimuli in detecting changes in retinal neurons in the early stages of streptozotocin (STZ)-induced rats (Kim et al, ARVO 2008). Here we assessed the utility of this method to detect early neuronal changes in a different animal model of DR, the STZ-mouse.
At 1.5 months of age, wildtype albino mice were subject to dark-adapted ERGs and divided into two groups. One group was made diabetic by intraperitoneal STZ (STZ-DM, n=7), while the other served as untreated control (n=8). Diabetes was confirmed by blood glucose levels > 400 mg/dL. At 3, 4, and 5 weeks post-diabetes, both groups of animals were dark adapted, and a scotopic intensity series (3.9x10-4 to137 cd s/m2) was recorded. Amplitudes and implicit times of a- and b-waves, and oscillatory potentials (OPs) were analyzed.
By 4 weeks, OP latencies of diabetic mice were significantly delayed in response to dim flash stimuli (<0.02 cd s/m2; p=0.01) and continued to show increased delays at 5 weeks. There were no differences in the a- and b-wave amplitudes between the two treatment groups; however, delays in the b-wave implicit time of diabetic mice was seen in response to dim flash at 4 weeks. While there were no significant differences in the dopamine level, there was a trend for decreased dopamine in the diabetic group.
Similar to previous findings, dim flash stimuli showed greater sensitivity than bright flash stimuli in detecting differences in neuronal function during early stages of DR in STZ-mice. Due to its known genome and the availability of mutant strains, using mouse models of DR will enable further investigation of the mechanisms underlying the neuronal changes seen in our study. Future studies will identify OP- generating pathways and histological changes affected by the disease.
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