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Early Functional and Morphologic Abnormalities in the Diabetic Nyxnob Mouse Retina
Matthew J Tarchick1, Parastoo Bassiri2, Rebecca M Rohwer2
1Louis Stokes Cleveland VA Medical Center, Cleveland, Ohio, United States 2Cole Eye Institute, Cleveland Clinic, Cleveland, Ohio, United States.
Investigative Ophthalmology & Visual Science
|July 2, 2016
Summary
Diabetic mice show reduced electroretinogram c-waves and slow PIII responses, indicating retinal pigment epithelium (RPE) changes rather than Müller glial cell dysfunction. These findings highlight hyperglycemia
Area of Science:
- Ophthalmology
- Neuroscience
- Diabetic Retinopathy Research
Background:
- The electroretinogram (ERG) c-wave originates from the retinal pigment epithelium (RPE) and Müller glial cells.
- Previous studies noted c-wave reductions in diabetic mouse models, but the specific cellular source remained unclear.
Purpose of the Study:
- To differentiate between RPE and Müller glial cell contributions to diabetes-induced c-wave reduction using a genetic approach.
- To investigate the impact of hyperglycemia on the slow PIII component of the ERG.
Main Methods:
- Utilized Nyxnob mice, which isolate the slow PIII response.
- Induced diabetes in Nyxnob mice using streptozotocin (STZ).
- Performed electroretinogram (ERG) and histological analyses at multiple time points post-STZ injection.
Main Results:
- Diabetes led to c-wave reduction starting at 1 week, persisting over time.
- Slow PIII amplitudes were initially unaffected but significantly reduced by week 2 in diabetic mice.
- Morphological changes in the RPE, including thickening and altered melanosome distribution, were observed in diabetic retinas.
Conclusions:
- Diabetes-induced c-wave reduction is not solely due to Müller glial cell changes.
- The distinct onset and magnitude of reductions in a-wave, slow PIII, and c-wave suggest varied mechanisms.
- Hyperglycemia likely causes primary alterations in the RPE, contributing to c-wave dysfunction in diabetic retinopathy.
