September 2016
Volume 57, Issue 12
Open Access
ARVO Annual Meeting Abstract  |   September 2016
Bright light suppresses form-deprivation myopia development through dopamine D1 receptor signaling activation in mice.
Author Affiliations & Notes
  • Xiangtian Zhou
    School of Ophthalmology and Optometry, Wenzhou Medical University, Wenzhou, Zhejiang, China
  • Si Chen
    School of Ophthalmology and Optometry, Wenzhou Medical University, Wenzhou, Zhejiang, China
  • Zhina Zhi
    School of Ophthalmology and Optometry, Wenzhou Medical University, Wenzhou, Zhejiang, China
  • Qingqing Ruan
    School of Ophthalmology and Optometry, Wenzhou Medical University, Wenzhou, Zhejiang, China
  • Fen Li
    School of Ophthalmology and Optometry, Wenzhou Medical University, Wenzhou, Zhejiang, China
  • Xiaoqing Li
    School of Ophthalmology and Optometry, Wenzhou Medical University, Wenzhou, Zhejiang, China
  • Jia Qu
    School of Ophthalmology and Optometry, Wenzhou Medical University, Wenzhou, Zhejiang, China
  • Footnotes
    Commercial Relationships   Xiangtian Zhou, None; Si Chen, None; Zhina Zhi, None; Qingqing Ruan, None; Fen Li, None; Xiaoqing Li, None; Jia Qu, None
  • Footnotes
    Support  NSFC(81422007, 81371047)
Investigative Ophthalmology & Visual Science September 2016, Vol.57, 5527. doi:
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      Xiangtian Zhou, Si Chen, Zhina Zhi, Qingqing Ruan, Fen Li, Xiaoqing Li, Jia Qu; Bright light suppresses form-deprivation myopia development through dopamine D1 receptor signaling activation in mice.. Invest. Ophthalmol. Vis. Sci. 2016;57(12):5527.

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

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Abstract

Purpose : Mechanisms of the inhibition of bright light to myopia developing is still unclear. This present study explored the role of dopamine D1 receptor (D1R) in the inhibition of form deprivation myopia (FDM) by bright light in mice.

Methods : Monocularly form-deprived (FD) mice were raised under normal light (NL, 100-200 lux) and bright light (BL, 2500-5000 lux) for 4 weeks. Retinal thickness and electroretinograms (ERGs) were measured 3 weeks after the experiment to exclude the possible light damages. The number of retinal cells expressing p-TH, c-fos, and cells co-expressing D1R and c-fos was calculated separately. A D1R antagonist, SCH39166 (SCH) was intraperitoneally injected for the FD and control groups to investigate its effect on FDM under normal and bright light environment. The refraction and ocular axial components were measured by an eccentric infrared photorefractor and real-time optical coherence tomography prior to and at the end of the experiment.

Results : There were no significant differences in retinal thickness and ERGs between NL and BL groups (p>0.05).The refraction in the BL group was more hyperopic than in the NL group after 4 weeks of experiment (+5.28±1.08D vs. +8.87±0.84D, p<0.05).The BL+FD group developed significantly less myopia than the NL+FD group (-4.65±0.94D vs. -8.43±0.74D, P<0.05). Bright light environment increased the number of cells expressing p-TH, c-fos and the number of cells co-expressing D1-R and c-fos. Intraperitoneal injection of SCH39166 effectively reversed the inhibiting effect of BL on FDM (NL+FD+SCH vs. BL+FD+SCH: -10.89±1.11D vs. -10.58±0.2D, p>0.05). The changes between axial length, vitreous chamber depth and refraction were also correlated.

Conclusions : Exposure to bright light can shift the refractive development towards hyperopia, and inhibit the development of FDM. Bright light increases retinal DA synthesis, and D1Ractivity.As theD1R antagonist eliminates the inhibition of bright light to FDM development. Those results indicate that the inhibitory effect of bright light on FDM probably mediated through activation ofD1R pathway.

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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