May 2005
Volume 46, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2005
Dark Adaptation and Deactivation of the Photoreceptor Response in Diabetic Rats
Author Affiliations & Notes
  • J.A. Phipps
    Optometry and Vision Sciences, University of Melbourne, Melbourne, Australia
  • P. Yee
    Anatomy and Cell Biology, University of Melbourne, Parkville, Australia
  • E.L. Fletcher
    Anatomy and Cell Biology, University of Melbourne, Parkville, Australia
  • A.J. Vingrys
    Optometry and Vision Sciences, University of Melbourne, Melbourne, Australia
  • Footnotes
    Commercial Relationships  J.A. Phipps, None; P. Yee, None; E.L. Fletcher, None; A.J. Vingrys, None.
  • Footnotes
    Support  NH & MRC grant (Australia) #208950 and Australian Research Council Linkage Project (LP0211474)
Investigative Ophthalmology & Visual Science May 2005, Vol.46, 3448. doi:
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      J.A. Phipps, P. Yee, E.L. Fletcher, A.J. Vingrys; Dark Adaptation and Deactivation of the Photoreceptor Response in Diabetic Rats . Invest. Ophthalmol. Vis. Sci. 2005;46(13):3448.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Abstract: : Purpose: To study the deactivation of the photoreceptor response and the recovery dynamics of the photoreceptoral dark current in normal and streptozotocin (STZ) diabetic rats. Methods: Two cohorts of Sprague–Dawley rats (aged 8 weeks) were randomly assigned to treatment (n = 39, STZ 50 mg/kg in trisodium citrate buffer, pH 4.5) and control (n = 37, 1 ml/kg of 0.01 M trisodium citrate buffer only, pH 4.5) groups, with function measured 12 weeks after the induction of diabetes using the electroretinogram (ERG). Deactivation of the active intermediate form of rhodopsin (metarhodopsin) was evaluated at four luminous exposures (0.9 – 2.2 log cd.s.m–2) using a variable interstimulus interval (ISI) paradigm (binary sequence from 0.5 to 128 s) and modelling as detailed by Pepperberg et al. (Vis Neurosci 1992). Recovery of the photoreceptoral dark current was evaluated at 90 s intervals for 30 min following an ∼20% pigment bleach. At each time point a paired–flash signal (1.4 log cd.s.m–2, ISI 0.8 s) was employed to extract the rod and cone waveforms. The time course of rod and cone recovery was modelled using the mechanisms described by Kennedy et al. (Neuron, 2001). Results: Diabetic animals displayed an average decrease of ∼24% in maximal rod PIII and ∼33% in cone PII amplitudes consistent with that reported by us elsewhere (Phipps et al. IOVS 2004). No difference was found in the rate of deactivation of metarhodopsin in STZ–treated rats. In contrast, although the rates of both phases of dark adaptation were unaffected by diabetes, normalised amplitudes showed that diabetic animals recovered significantly faster to baseline (p<0.01) than did controls for both rod and cone responses. Conclusions: Photoreceptor deactivation and the kinetics of dark adaptation are not altered after 12 weeks of STZ diabetes. However, the faster relative recovery found in diabetes following bleach, in the presence of normal pigment dynamics, implies a decreased pigment density in diabetic animals for both rods and cones.

Keywords: electroretinography: non-clinical • diabetes • photoreceptors: visual performance 
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