July 2018
Volume 59, Issue 9
Open Access
ARVO Annual Meeting Abstract  |   July 2018
Combined effects of bright light and intravitreal atropine on retinal dopamine release in chickens
Author Affiliations & Notes
  • Ute Mathis
    Section of Neurobiology of the Eye, Ophthalmic Research Institute, Tuebingen, Germany
  • Marita P Feldkaemper
    Section of Neurobiology of the Eye, Ophthalmic Research Institute, Tuebingen, Germany
  • Min Wang
    Section of Neurobiology of the Eye, Ophthalmic Research Institute, Tuebingen, Germany
  • Frank Schaeffel
    Section of Neurobiology of the Eye, Ophthalmic Research Institute, Tuebingen, Germany
  • Footnotes
    Commercial Relationships   Ute Mathis, None; Marita Feldkaemper, None; Min Wang, None; Frank Schaeffel, None
  • Footnotes
    Support  This study was supported by the STZ Biomedical Optics and the Medical Faculty, University of Tuebingen.
Investigative Ophthalmology & Visual Science July 2018, Vol.59, 685. doi:
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      Ute Mathis, Marita P Feldkaemper, Min Wang, Frank Schaeffel; Combined effects of bright light and intravitreal atropine on retinal dopamine release in chickens. Invest. Ophthalmol. Vis. Sci. 2018;59(9):685.

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

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Abstract

Purpose : Atropine is well known to inhibit myopia progression in animal models and children but the underlying mechanisms remain elusive. Atropine stimulates the release of nitric oxide (Carr and Stell., 2016) and perhaps dopamine (Schwahn et al., 2000) . Both agents represent light signals for the retina and may mimic exposure to bright light. We have studied how light and intravitreal atropine interact to control dopamine release from the chicken retina.

Methods : Exp.1: Atropine sulfate monohydrate (250µg /25µl saline) was intravitreally injected into one eye in 20 chicks. The fellow eye received saline. Dopamine and its metabolites were measured in vitreous, 1, 1.5, 2, 3 and 4 hours after injection, using HPLC-ED. Exp. 2: In 12 chicks, atropine was injected as above but the chicks were subsequently transferred into either bright light (8500 lux, n=6) or office light (500 lux, n=6) for 1.5 hours before dopamine was measured.

Results : Exp. 1: Vitreal dopamine content in atropine-injected eyes was elevated compared to saline-injected fellow eyes, 1h after the injections (saline 0.06+0.03 ng/0.1mg wet weight vs. atropine 0.35+0.13, p<0.02, paired t-test). It peaked at around 2h following injections and returned to baseline after 4h. Interestingly, there was a clear contralateral effect with elevated dopamine release by 50% also in fellow eyes. Exp. 2: While the effect of bright light on dopamine release was not significant in the saline injected eyes, it was significant in eyes that had received atropine (office light 0.50+0.28ng/0.1mg wet weight vs. bright light 0.85+0.22, p<0.04, unpaired t-test). Comparing all atropine injected eyes to all saline injected eyes, atropine again had a stimulatory effect on dopamine release (saline 0.42+0.16ng/1mg wet weight vs. atropine 0.67+0.30, p<0.01, paired t-test).

Conclusions : Atropine stimulates release of dopamine from the retina, suggesting that it may act as a light signal for the retina. Bright light itself did not increase dopamine release in saline-injected eyes but also previous authors (Cohen et al., 2012) observed little differences in vitreal DOPAC between 500 and 5000 lux. In combination with atropine, the effects of bright light became conspicuous. In summary, both bright light and atropine can interact to increase dopamine release from the chicken retina and may represent one of the mechanisms by which atropine inhibits myopia.

This is an abstract that was submitted for the 2018 ARVO Annual Meeting, held in Honolulu, Hawaii, April 29 - May 3, 2018.

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