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A.J. Vingrys, A.E. Weymouth, A.J. Sinclair; Does Altered Membrane Biophysics Explain in vivo Retinal Functional Deficits From omega–3 Deficiency? . Invest. Ophthalmol. Vis. Sci. 2005;46(13):3447.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: Omega–3 PUFA deficiency has been reported to produce deficits in rod dark current amplitudes (RmPIII) and kinetics (sensitivity, S) in vivo. However, studies in reconstituted omega–3 deficient membranes in vitro predict delays in onset of rod activation (td). To our knowledge, the changes in td have never been rigorously tested in vivo, so this study investigated whether a delay of rod activation exists in rats deprived of omega–3 PUFA in their diet. Methods: Adult Sprague–Dawley rats were raised on either omega–3 sufficient (Suf) or deficient (Def) diets from conception (n = 32/diet). Twin flash (interstimulus interval 800 ms) electroretinograms were obtained from anaesthetised animals (ketamine:xylazine anaesthesia, 35:5 mg/kg im) at 5, 10 and 20 weeks of age and rod–derived waveforms were extracted. Ensembles of rod–extracted a–waves (0.4 – 1.9 log cd·s·m–2) were modelled to determine RmPIII, S and td. Retinal phospholipid profiles were assayed at each age. Results: DHA proportions in retinal phospholipids were significantly altered by the dietary manipulation at all ages (p < 0.01). Consistent with in vitro predictions, dark current amplitude (RmPIII) was significantly reduced at all ages (–16%, –14%, –30%, p < 0.01), whereas sensitivity was significantly reduced at 10 and 20 weeks only (–0.12, –0.13 log units, p < 0.001) in omega–3 deficient animals. Diet showed a significant interaction with age (p < 0.001) for the delay parameter (td), giving non–significant changes at 5 and 10 weeks (p > 0.05) and a 0.22 ms (7.3%) delay at 20 weeks (p < 0.01). Conclusions: Our data suggest multiple, age–dependent mechanisms underlie the retinal functional deficits in omega–3 PUFA deprivation. Our young (≤ 10 weeks) animals have significant changes in tissue omega–3 profiles, which induce reductions in RmPIII and S in the presence of a normal delay (td). This finding is compelling given our adequate power (0.96) to detect a td delay of 0.3 ms (10% change) expected from in vitro studies. The pattern of losses present at 20 weeks alone showed some similarity to those predicted by changes to membrane biophysics.
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