Bright Light Suppresses Form-Deprivation Myopia Development With Activation of Dopamine D1 Receptor Signaling in the ON Pathway in Retina

Chen, Si; Zhi, Zhina; Ruan, Qingqing; Liu, Qingxia; Li, Fen; Wan, Fang; Reinach, Peter S.; Chen, Jiang‐Fan; Qu, Jia; Zhou, Xiangtian

doi:10.1167/iovs.16-20402

Cited by 86 publications

(76 citation statements)

References 53 publications

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“…iii) based in part on recent finding from mouse model of myopia, we suggest that differential activation of dopamine receptors in distinct vision pathways (despite similar expression levels) and neural circuits (Chen et al, 2017), may also contribute to different functional outcomes. Coupled with cellular biomarkers and molecular approaches, insights from mouse genetic manipulation would provide complementary and fresh view for some of the long-held views on myopia development.…”

Section: Role Of D1-like and D2-like Receptors In Myopia Developmentmentioning

confidence: 75%

“…Furthermore, the light hypothesis, i.e. light-stimulated DA antagonizes myopia development (Rose et al, 2008) has been supported by a number of studies that show outdoor activity and/or bright light inhibits myopia, potentially through DA-mediated mechanisms (Ashby et al, 2009; Chen et al, 2017; Cohen et al, 2011; Cohen et al, 2012; Li et al, 2014; Morgan et al, 2012; Smith et al, 2012; Wang et al, 2015; Wu et al, 2013). The evidence from pharmacological and genetic studies has provided more details regarding how light or visual input controls retinal DA signaling and contributes to refractive development (for a recent review, see (Feldkaemper and Schaeffel, 2013)).…”

Section: Introductionmentioning

confidence: 98%

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Dopamine signaling and myopia development: What are the key challenges

Zhou

Pardue

Iuvone

et al. 2017

Progress in Retinal and Eye Research

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In the face of an “epidemic” increase in myopia over the last decades and myopia prevalence predicted to reach 2.5 billion people by the end of this decade, there is an urgent need to develop effective and safe therapeutic interventions to slow down this “myopia booming” and prevent myopia-related complications and vision loss. Dopamine (DA) is an important neurotransmitter in the retina and mediates diverse functions including development, visual signaling, and refractive development. Inspired by the convergence of epidemiological and animal studies in support of the inverse relationship between outdoor activity and risk of developing myopia and by the close biological relationship between light exposure and dopamine release/signaling, we felt it is timely and important to critically review the role of DA in myopia development. This review will revisit several key points of evidence for and against DA mediating light control of myopia: 1) the causal role of extracellular retinal DA levels, 2) the mechanism and action of dopamine D1 and D2 receptors and 3) the roles of cellular/circuit retinal pathways. We examine the experiments that show causation by altering DA, DA receptors and visual pathways using pharmacological, transgenic, or visual environment approaches. Furthermore, we critically evaluate the safety issues of a DA-based treatment strategy and some approaches to address these issues. The review identifies the key questions and challenges in translating basic knowledge on DA signaling and myopia from animal studies into effective pharmacological treatments for myopia in children.

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Section: Role Of D1-like and D2-like Receptors In Myopia Developmentmentioning

confidence: 75%

Section: Introductionmentioning

confidence: 98%

Dopamine signaling and myopia development: What are the key challenges

Zhou

Pardue

Iuvone

et al. 2017

Progress in Retinal and Eye Research

Self Cite

229

203

View full text Add to dashboard Cite

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“…49 Similarly, preliminary studies indicated the D1R agonist SKF 38393 inhibited FDM, whereas the D1R antagonist SCH 39166 enhanced FDM in mice (Zhou X, et al IOVS 2014;55:ARVO E-Abstract 3038). 30 However, other studies in chickens and tree shrews found that the development of FDM was not affected by intravitreal injection of the D1R antagonist SCH 23390. 50,51 In the present study, the mouse D1R gene was deleted throughout the body during early development, and the D1R-KO mice exhibited growth retardation and small body weight compared with WT mice due to reduced food and water intake, as reported previously.…”

Section: D1r-dependent Mechanism Of Apomorphine In Myopiamentioning

confidence: 94%

“…The injection volume in all groups was 1 lL/g body weight. The pharmacologic doses were chosen based on our 22,30 and other studies.…”

Section: Preparation For Drug Injectionmentioning

confidence: 99%

“…In contrast to D2Rs, inactivation of D1Rs by the D1R antagonist SCH39166 inhibited the development of myopia in mice. 30 Because of the complexity and inherent limitations of dopamine receptor pharmacology, a more direct approach to dissecting the roles of D2Rs and D1Rs in myopia development would be helpful. Thus, the use of genetic KO mice may provide complementary and more definitive insight regarding the roles of D2Rs and D1Rs.…”

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confidence: 99%

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Dopamine D1 Receptors Contribute Critically to the Apomorphine-Induced Inhibition of Form-Deprivation Myopia in Mice

Huang

Zhang

Wang

et al. 2018

Invest. Ophthalmol. Vis. Sci.

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PURPOSE. To determine the roles of dopamine D2 receptors (D2Rs) and dopamine D1 receptors (D1Rs) in the inhibition of form-deprivation myopia (FDM) by the nonselective dopamine agonist apomorphine (APO) in D2R-knockout (D2R-KO) and D1R-KO mice. METHODS.Retinal layer thicknesses and electroretinograms (ERGs) were analyzed in KO mice and in D2R and D1R antagonist-treated mice. D2R-KO or D1R-KO mice and wild-type (WT) littermates were subjected to form deprivation during postnatal weeks 5 to 8. Both groups were intraperitoneally injected daily with either APO (5 lg/g body weight) dissolved in 1 lg/ lL ascorbic acid or vehicle alone. Refraction, vitreous chamber depth (VCD), and axial length (AL), among other parameters, were measured prior to and at the end of the treatment period.RESULTS. The retinal layer thicknesses and ERGs in KO mice were similar to those treated with D2R and D1R antagonists. APO administration in WT mice inhibited the development of FDM by approximately 80%. FDM in D2R-KO mice was inhibited approximately 50% compared with WT mice and was further inhibited by APO to a level similar to that in APO-treated WT mice. FDM development in D1R-KO mice was similar to that in WT mice and was not affected by APO administration. The changes in VCD and AL were consistent with refraction data.CONCLUSIONS. In mice, APO-mediated FDM inhibition was abolished by D1R KO but not D2R KO. This indicates the specificity of D1Rs for the pharmacologic inhibitory effect of APO on FDM and a nonessential role of D2Rs in this process in mice.

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