May 2008
Volume 49, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2008
Altered Pupil Light Responses in the Rpe65 R91W Mice
Author Affiliations & Notes
  • Y. Arsenijevic
    Unit of Gene Therapy & Stem Cell Biology, Jules-Gonin Eye Hospital Univ. Lausanne, Lausanne, Switzerland
  • C. Kostic
    Unit of Gene Therapy & Stem Cell Biology, Jules-Gonin Eye Hospital Univ. Lausanne, Lausanne, Switzerland
  • A. P. Bemelmans
    Unit of Gene Therapy & Stem Cell Biology, Jules-Gonin Eye Hospital Univ. Lausanne, Lausanne, Switzerland
  • M. Samardzija
    University of Zürich, Zürich, Switzerland
  • S. Grozdanic
    Iowa State University, Ames, Iowa
  • R. Kardon
    University of Iowa and Veterans Administration Medical Center., Iowa City, Iowa
  • A. Kawazaki
    Unit of Neuro-ophthalmology, Jules-Gonin Eye Hospital, Lausanne, Switzerland
  • S. V. Crippa
    Unit of Gene Therapy & Stem Cell Biology, Jules-Gonin Eye Hospital Univ. Lausanne, Lausanne, Switzerland
  • Footnotes
    Commercial Relationships  Y. Arsenijevic, None; C. Kostic, None; A.P. Bemelmans, None; M. Samardzija, None; S. Grozdanic, None; R. Kardon, None; A. Kawazaki, None; S.V. Crippa, None.
  • Footnotes
    Support  Novartis Foundation
Investigative Ophthalmology & Visual Science May 2008, Vol.49, 2983. doi:
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      Y. Arsenijevic, C. Kostic, A. P. Bemelmans, M. Samardzija, S. Grozdanic, R. Kardon, A. Kawazaki, S. V. Crippa; Altered Pupil Light Responses in the Rpe65 R91W Mice. Invest. Ophthalmol. Vis. Sci. 2008;49(13):2983.

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

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Abstract

Purpose: : Setting up pupil light reflex (PLR) recordings to assess visual function in mouse models of retinal degeneration.

Methods: : Adult SV129/S6 (controls) and Rpe65 R91W mice (1 and 3 months old) expressing an altered form of the RPE65 protein leading to progressive retinal degeneration (Samardzija et al., 2007) were anesthetized with xylazine-ketamine mixture. The pupil contraction to a 50 ms white light stimulus of increasing intensity (0.225 to 1500 lux) was recorded using a NeurOptics A1000 pupillometer for small animals (San Clemente, CA, US).

Results: : In both groups, increasing light intensity resulted in greater pupillary contraction amplitude. Variability of the inter- and intra-animal pupil responses precluded assessment of significant difference between the groups. Nonetheless, Rpe65 R91W mice more often failed to respond to light stimulation, independently to light intensity, and the cumulative performance of pupil constriction was calculated. Over the 50 total stimuli applied, the Rpe65 R91W mice average number of responses was only 10 ± 4.5, markedly reduced in comparison to 48 ± 0.5 responses of the control group (p<0.001). The pupil response waveforms were not observably dissimilar between groups but specific parameters of the kinetic response are still under analysis.

Conclusions: : During slow retinal degeneration, different rates of cell death can occur between animals and lead to varying levels of visual function loss during a specific time period. For 1 and 3 months old mice, the numberof PLR responses to the stimulation protocol were significantly reduced in the Rpe65 R91W mice, suggesting that this may be one measure of function which correlates with the histologic loss of photoreceptors at this age as well as with the low level of the chromophore. The performance of PLR (i.e. number of responses over the total number of stimuli) can be an objective and reliable parameter to evaluate visual function in mouse model of slow retinal degeneration.

Keywords: retinal degenerations: hereditary • pupillary reflex • photoreceptors 
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