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V. H. Wong, A. J. Vingrys, B. V. Bui; Müller Cell Function in STZ-Induced Diabetic Rat Retina Isolated Using Barium Chloride. Invest. Ophthalmol. Vis. Sci. 2010;51(13):5763.
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We consider whether the Müller cell contribution to retinal function is affected in early stages of streptozotocin (STZ) diabetes.
Electroretinogram (ERG) responses were measured in anaesthetized (60:5 mg/kg Ketamine:Xylazine), dark-adapted (>12 hours) adult Long-Evans rats 5 weeks following injection of citrate buffer (n = 6) or streptozotocin (STZ, n = 8, 65 mg/kg, blood glucose: >15mmol/L). ERGs were recorded (-5.66 to 2.28 log cd.s.m-2) 40 minutes after intravitreal injection of barium chloride (BaCl2, 2 mM, 2 µl) to inhibit inward rectifying potassium channels, or dH2O (2 µl) in the contralateral eye to act as an internal control. At 60 minutes, L-amino-4-phosphonobutyric acid (APB, 1 mM, 3 µl) and cis-2,3-piperidinedicarboxylic acid (PDA, 5 mM, 2 µl) were injected into both eyes to inhibit post-receptoral function and expose the a-wave (in BaCl2 eyes) and a-wave/slow-P3 (in dH2O eyes). After a further 40 minutes, ERGs were recorded. ON-bipolar cell (b-wave) and Müller cell responses (slow-P3, at a fixed time of 40 ms) are expressed relative to photoreceptoral output (b-/a-wave, slow-P3/a-wave). Two-tailed, unpaired t-tests were used to evaluate differences between citrate and STZ groups (mean ± SEM).
Under normal conditions, b-/a-ratio was similar in citrate (1.53 ± 0.07) and STZ groups (1.66 ± 0.12, P = 0.35). BaCl2, produced significantly larger b/a-ratio in STZ animals (3.37 ± 0.10) compared with citrate controls (3.04 ± 0.10, P < 0.05). The normalization for the a-wave amplitude output means that the enhanced b-/a-ratio in STZ-treated ERGs could be due to the loss of a larger negative Müller cell slow-P3, a possibility tested by introducing APB/PDA. Instead of the expected larger slow-P3 in STZ-eyes with APB/PDA, these drugs revealed a significantly smaller slow-P3/a-ratio in the STZ-group (0.89 ± 0.05) compared with citrate controls (1.07 ± 0.01, P = 0.01).
The effect of BaCl2 is greater in STZ-eyes. This enhancement cannot be explained by the loss of a larger Müller cell slow-P3 component. These outcomes suggest that potassium buffering is altered in diabetic eyes early in the disease process.
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