Abstract
Purpose:
In various species, reduced retinal dopamine (DA) levels are thought to mediate the development of myopia. However, recent evidence shows that in the C57BL/6 mouse, retinal DA levels are unaltered when form-deprivation myopia is developed. Here, to further explore the role of retinal DA in mouse eye growth, we examined whether refractive development could be disturbed by destroying retinal DA pathway in this mouse strain.
Methods:
6-hydroxydopamine (6-OHDA, 50 μg) was intravitreally applied to the right eye using a micro-injector, and the left eye serves as the control. Refractive errors were measured using an automated eccentric infrared photorefractor, in animals raised in normal visual environment, or in those with the injected eye wearing an occluder for 4 weeks to induce form-deprivation myopia. The levels of retinal DA and its primary metabolite 3,4-dihydroxyphenylacetic acid (DOPAC) were assessed by HPLC analysis.
Results:
Administration of 6-OHDA significantly reduced retinal DA levels by 40-80%, and the effect lasted for at least 31 days. With normal visual experience, the 6-OHDA-injected eyes became markedly myopic relative to their fellow eyes (~6D of interocular difference). Furthermore, in injected eyes, form-deprivation did not induce further myopic shifts, nor did it cause further reduction in retinal DA and DOPAC levels.
Conclusions:
An intact retinal dopaminergic system, including healthy dopaminergic amacrine cells and complete retinal DA stores, is essential for both normal refractive development and the generation of form-deprivation myopia in the C57BL/6 mouse. In this mouse strain, refractive development could be interfered by reducing retinal DA levels dramatically, even though the generation of form-deprivation myopia is not associated with retinal DA levels.