September 2016
Volume 57, Issue 12
Open Access
ARVO Annual Meeting Abstract  |   September 2016
Ascorbic acid, and not L-DOPA, protects against form-deprivation myopia in retinal degeneration mouse models.
Author Affiliations & Notes
  • Erica Landis
    Ophthalmology, Emory University, Atlanta, Georgia, United States
    Neuroscience, Emory University, Atlanta, Georgia, United States
  • Hanna Park
    Ophthalmology, Emory University, Atlanta, Georgia, United States
  • Ranjay Chakraborty
    Ophthalmology, Emory University, Atlanta, Georgia, United States
  • Curran Sidhu
    Ophthalmology, Emory University, Atlanta, Georgia, United States
  • P. Michael Iuvone
    Ophthalmology, Emory University, Atlanta, Georgia, United States
    Pharmacology, Emory University, Atlanta, Georgia, United States
  • Machelle T Pardue
    Biomedical Engineering, Georgia Institute of Technology, Atlanta, Georgia, United States
    Center for Visual and Neurocognitive Rehabilitation, Veterans Affairs Medical Center, Atlanta, Georgia, United States
  • Footnotes
    Commercial Relationships   Erica Landis, None; Hanna Park, None; Ranjay Chakraborty, None; Curran Sidhu, None; P. Michael Iuvone, None; Machelle Pardue, None
  • Footnotes
    Support  NIH NEI R01 EY016435, R01 EY004864, P30 EY006360, T32 EY007092-29, Research to Prevent Blindness, and Dept. of Veterans Affairs Rehabilitation R&D Service Research Career Scientist Award C9257S
Investigative Ophthalmology & Visual Science September 2016, Vol.57, No Pagination Specified. doi:
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      Erica Landis, Hanna Park, Ranjay Chakraborty, Curran Sidhu, P. Michael Iuvone, Machelle T Pardue; Ascorbic acid, and not L-DOPA, protects against form-deprivation myopia in retinal degeneration mouse models.. Invest. Ophthalmol. Vis. Sci. 201657(12):.

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

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Abstract

Purpose : Mouse models of retinal degeneration have shown increased susceptibility to form deprivation myopia, potentially due to decreased dopamine (DA) turnover (Park et al., 2013) or loss of dopaminergic amacrine cells (DACs; Ivanova et al., 2015). The purpose of this work is to test whether systemic injections of the DA precursor, L-3,4-dihydroxyphenylalanine (L-DOPA) will protect against form deprivation (FD) myopia in wild-type and retinal degeneration mice.

Methods : Susceptibility to FD myopia was measured beginning at post-natal day 28 (P28) in Pde6brd10/rd10 (rd10) mice and age-matched C57BL/6J wild-type (WT) mice. A subset of animals was given monocular FD lenses following baseline measurements. At P28, mice received daily systemic injections of L-DOPA only (n=17), L-DOPA + the vehicle, ascorbic acid (AA)( n=18-25), or AA only (n=18-21). Weekly measurements of refractive error, corneal curvature, and ocular biometry were performed until P42, using photorefraction, keratometry, and spectral-domain optical coherence tomography. At P44 retinas were collected to measure dopamine (DA) and its metabolite 3,4-dihydroxyphenylacetic acid (DOPAC) with HPLC.

Results : WT mice exposed to FD developed a significant myopic shift (right-left eye) with AA only treatment (-3.54 ± 1.14D); that was significantly decreased by L-DOPA + AA (0.283 ± 0.588D, p<0.01). Rd10 mice showed the opposite response such that AA only treatment significantly reduced the myopic shift in response to FD (-0.769 ± 0.464D) compared to L-DOPA + AA (-3.206 ± 0.734) or L-DOPA only treatments (-5.752 ± 0.761D, p<0.05). No significant changes were seen in corneal curvature or ocular parameters.

Conclusions : Similar to findings in other animals, L-DOPA treatment protects WT mice from FD myopia. However, L-DOPA treatments did not halt or slow FD myopia in rd10 mice, while AA only treatments completely eliminated the myopic shift. We hypothesize that L-DOPA is not protective effect in rd10 mice due to dysfunctional DACs that aren’t able to convert L-DOPA to DA. Furthermore, the anti-oxidant effects of AA on extracellular DA (Neal et al., 1999) may preserve DA in rd10 retinas that is not rapidly degraded by defective DACs. We will confirm this hypothesis with the measurement of dopamine and DOPAC levels with HPLC in each treatment group.

This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.

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