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Xiangtian Zhou, Weiwei Xiong, Furong Huang, JInglei Yang, Jia Qu; C57BL/6 mouse eyes treated by dopamine D1 receptor agonist and antagonist during form deprivation: an opposite effect on axial length and refractive development. Invest. Ophthalmol. Vis. Sci. 2014;55(13):3038.
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© ARVO (1962-2015); The Authors (2016-present)
Dopaminergic activities in the eye have been shown to modulate development of form deprivation myopia (FDM). However, the mechanism of dopamine receptors involved in FDM is complex. In this study, we investigated effects of dopamine D1 receptor (DRD1) on the development of refraction and axial components of the eyes treated with form deprivation using selective DRD1 agonist and antagonist.
Four-week-old C57BL/6 mice (n=245) raised in normal visual environments or form deprivation received daily intraperitoneal injection of either SKF38393 (DRD1 agonist, n=121) or SCH39166 (DRD1 antagonist, n=124) for four weeks. Each of the groups was divided into 4 sub-groups including control, vehicle and drug treatments with two different dosages. The refraction, corneal radius of curvature and axial components of the eye were measured in all animals prior to and after the treatments.
After four weeks of treatment, eyes treated with SKF38393 showed a dose dependent inhibition to the development of FDM with a slower increase in vitreous chamber depth and axial length compared to the vehicle group. In contrast, SCH39166-treated animals showed a dose dependent promotion of FDM with a more rapid increase in vitreous chamber depth and axial length compared to the vehicle group. No significant differences in corneal radius of curvature, anterior chamber depth or lens thickness among the different groups were found during the experimental period. The refraction and axial components of the eyes raised in normal visual environments were not affected neither by SKF38393 nor SCH39166.
DRD1 agonist and antagonist exert opposite effects on refractive development and ocular growth during form deprivation. An activation of DRD1 can inhibit the development of FDM in C57BL/6 mice.
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