April 2010
Volume 51, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2010
Rhodopsin Recovery Dysfunction in Young RCS Rats: Electrophysiological Study
Author Affiliations & Notes
  • A. D. Baryluk
    Eye Hospital, Medical University of Lublin, Lublin, Poland
    Centre for Ophthalmology, University of Tuebingen, Tuebingen, Germany
  • S. Thaler
    Centre for Ophthalmology, University of Tuebingen, Tuebingen, Germany
  • R. Rejdak
    Eye Hospital, Medical University of Lublin, Lublin, Poland
    Centre for Ophthalmology, University of Tuebingen, Tuebingen, Germany
  • T. arnowski
    Eye Hospital, Medical University of Lublin, Lublin, Poland
  • E. Zrenner
    Centre for Ophthalmology, University of Tuebingen, Tuebingen, Germany
  • Footnotes
    Commercial Relationships  A.D. Baryluk, None; S. Thaler, None; R. Rejdak, None; T. arnowski, None; E. Zrenner, None.
  • Footnotes
    Support  Tistou und Charlotte Kerstan Stiftung
Investigative Ophthalmology & Visual Science April 2010, Vol.51, 5573. doi:
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      A. D. Baryluk, S. Thaler, R. Rejdak, T. arnowski, E. Zrenner; Rhodopsin Recovery Dysfunction in Young RCS Rats: Electrophysiological Study. Invest. Ophthalmol. Vis. Sci. 2010;51(13):5573.

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Abstract

Purpose: : Retinal dystrophy in the Royal College of Surgeons (RCS) rats, related to the impairment in phagocytosis of shed rod outer segments by retinal pigment epitelium (RPE) cells, results in photoreceptor cell death, which may be evident already at 16th postnatal day (P16). The aim of this functional investigation was to test by means of electrophysiological (ERG) method, changes in the post-bleaching rhodopsin recovery and their time course at early phase of retinal degeneration in young RCS rats.

Methods: : Ganzfeld ERGs (Diagnosys Espion e2) were recorded in young RCS rats (n=10) at different postnatal time points (P17-18, P19-20, P21-23, P25-26, P27, P28-30). Results were compared to the ERGs obtained from healthy Brown-Norway (BN) rats (n=4) at P19, P23 and P30. Stimuli of increasing luminance (0.000003-0.3 cd.s/m2) were applied in scotopic conditions to derivate the intensity-response relationship of b-wave amplitude. Next, the recovery of rod semi-saturated b-wave amplitude was evaluated with a single flash of 0.003 cd.s/m2 delivered before and every 2 minute for 50 min after exposure to bleaching ligh (400 cd/m2, 30 sek). Finally, cone responses were recorded in photopic conditions with single flash and 20Hz flicker.

Results: : Scotopic and photopic ERG amplitudes in dystrophic RCS rats showed a small increase between P17-18 and P19-20, following by a decrease in dark adapted ERGs at P27-30. RCS rats revealed a distinct impairment in recovery of rod response when followed up to 50 min after bleaching: b-wave amplitudes received on average 55.0±8.4 µV (at P17-18), 73.4±41.6 (P19-20), 99.3±6.7 (P21-23), 59.2±20.5 (P25-26), 58.9±16.9 (P27) and 61.5±22.5 µV (P28-30). At the same time points, pre-bleaching rod b-wave amplitudes were: 188.3±61.6 , 330.6±87.7 , 353.3±75.9 , 301.0±148.5 , 137.4±65.0 and 122.0±91.0 µV (mean±SD). Healthy BN rats had slightly deficient rod recovery at P19 (about 80% of pre-bleaching values in b-wave amplitude), and full recovery at P23 and P30.

Conclusions: : Our results in the RCS rats indicate, that the ERG might be an usefull test for the early detection of distinct abnormalities in rhodopsin recovery, preceding the significant loss of photoreceptors function in inherited retinal degenerations.

Keywords: electroretinography: non-clinical • electrophysiology: non-clinical • retinal degenerations: hereditary 
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