Effects of induced myopia and hyperopia on dopaminergic and serotonergic amacrine neurons in chick retina

Abstract

The ametropias, myopia and hyperopia, are refractive errors which can be experimentally induced in young animals by manipulating their early visual experience. Myopia and hyperopia result from abnormal ocular growth mechanisms, and the control signals are believed to originate from within the eye itself.

In this study, unilateral application of convex lenses, concave lenses, and translucent goggles over the eyes of newly-hatched chicks respectively produced defocus-induced hyperopia (DIH), defocus-induced myopia (DIM), and form deprivation myopia (FDM). Treatment rapidly produced refractive errors and changes in eye size within 6 to 10 days. The effects of induced ametropias on retinal serotonergic and dopaminergic amacrine neurons were assessed on a quantitative and qualitative basis. Cell distributions and morphology in immunohistochemically labelled wholemount retinae were examined using confocal laser scanning microscopy. Neurochemical levels were measured using high pressure liquid chromatography (HPLC).

Induced ametropias produced changes in: (1) serotonergic amacrine cell distribution. (2) dopaminergic amacrine cell morphology, and (3) levels of dopamine and 3,4-dihydroxyphenylacetic acid (DOPAC). With respect to sertonogergic amacrine cell numbers, there was evidence of redistribution within the retina. In the central retina, FDM produced significant decreases in serotonergic cell numbers, while DIH provoked significant localized increases. These changes in serotonergic cell number appeared to be correlated with the magnitude of the induced refractive error. There were no changes in dopaminergic amacrine cell numbers. Dendritic morphology was assessed by recording optical sections across individual dopaminergic amacrine cells, then stacking these confocal images into composite overlays. FDM provoked increases in dendritic field spreads and dendritic branching in treated dopaminergic amacrines relative to control. Conversely, DIH produced consistent decreases in field size, staining intensity, and dendritic branching. HPLC analysis showed that both FDM and DIH caused significant decreases in retinal dopamine and DOPAC levels in treated eyes relative to controls. These changes were mainly localized within the central retina. There were no conclusive changes in the levels of serotonin and its metabolite 5-hydroxyindoleacetic acid, although slight decreases were noted in FDM, while DIH caused slight increases.

There is a high degree of neural plasticity within the young eye. Results from this study suggest that dopamine and serotonin may contribute, in a localized manner, to the ocular growth mechanisms which regulate the development of refractive errors.