May 2007
Volume 48, Issue 13
ARVO Annual Meeting Abstract  |   May 2007
Retinal Defects Influence Unmanipulated Refractive Development in Mice
Author Affiliations & Notes
  • A. E. Faulkner
    Rehab R & D, Atlanta VA Medical Center, Decatur, Georgia
  • H. Y. Choi
    Rehab R & D, Atlanta VA Medical Center, Decatur, Georgia
    Ophthalmology, Pusan National University, Pusan, Republic of Korea
  • M. K. Kim
    Rehab R & D, Atlanta VA Medical Center, Decatur, Georgia
  • M. A. McCall
    Psychological and Brain Science, University of Louisville, Louisville, Kentucky
  • P. M. Iuvone
    Emory University, Atlanta, Georgia
  • M. T. Pardue
    Rehab R & D, Atlanta VA Medical Center, Decatur, Georgia
    Emory University, Atlanta, Georgia
  • Footnotes
    Commercial Relationships A.E. Faulkner, None; H.Y. Choi, None; M.K. Kim, None; M.A. McCall, None; P.M. Iuvone, None; M.T. Pardue, None.
  • Footnotes
    Support Emory University Research Committee, Department of Veteran's Affairs, and Research to Prevent Blindness
Investigative Ophthalmology & Visual Science May 2007, Vol.48, 4419. doi:
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      A. E. Faulkner, H. Y. Choi, M. K. Kim, M. A. McCall, P. M. Iuvone, M. T. Pardue; Retinal Defects Influence Unmanipulated Refractive Development in Mice. Invest. Ophthalmol. Vis. Sci. 2007;48(13):4419.

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

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Purpose:: There is increasing evidence that the mechanisms controlling refractive development originate in the retina with detection of image blur. To further explore these retinal mechanisms, we are investigating refractive development in murine models with retinal defects. Here we examined mutant mouse models resulting in specific changes in retinal function: nob, GABAC receptor null, and rd1. Nob mice have a defect in ON pathway transmission; GABAC null mice have defects in neurotransmitter signaling; while rd1 mice have rapid degeneration of photoreceptors caused by a mutation in the gene encoding a PDE subunit.

Methods:: All mice were housed under normal laboratory conditions on a 12:12 light:dark cycle (50-200 lux). Refractions were obtained from nob (n=27), GABAC null (n=8), rd1 (n=5) and wild-type C57Bl/6J (n=9) mice using an automated photorefractor at 28 and 42 days of age. Refractions were obtained from awake mice to determine a refractive range and then anaesthetized and quickly refracted again to obtain a more accurate measurement.

Results:: The four strains of mice tested had significantly different refractive errors without any experimental visual manipulations (Repeated measures ANOVA F(3,45) = 108.4, p<0.001). From 28 to 42 days of age, C57Bl/6J mice had refractive errors from +6.9 ±0.5 to +8.5 ±0.3 dioptres (D). Nob and rd1 mice were ~2 D significantly more hyperopic than C57 mice at both timepoints (p<0.001). In contrast the GABAC null mice were ~5 D more myopic than C57 mice at both timepoints (p<0.001). All mice had a trend towards more hyperopic refractions with age.

Conclusions:: Collectively these results suggest that normal retinal function drives the development of emmetropia. Disruptions in retinal transmission may affect stop signal pathways, leading to changes in eye growth and refractive development.

Keywords: retina • myopia • refractive error development 

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