Abstract
Animal models have demonstrated a link between dysregulation of the retinal dopamine system and the development of myopia (short-sightedness). We have previously demonstrated that topical application of levodopa in chicks can inhibit the development of form-deprivation myopia (FDM) in a dose-dependent manner. Here, we examine whether this same protection is observed in lens-induced myopia (LIM), and whether levodopa’s protection against FDM and LIM occurs through a dopamine D1- or D2-like receptor mechanism. To do this, levodopa was first administered daily as an intravitreal injection or topical eye drop, at one of four ascending doses, to chicks developing LIM. Levodopa’s mechanism of action was then examined by co-administration of levodopa injections with D1-like (SCH-23390) or D2-like (spiperone) dopamine antagonists in chicks developing FDM or LIM. For both experiments, levodopa’s effectiveness was examined by measuring axial length and refraction after 4 days of treatment. Levodopa inhibited the development of LIM in a dose-dependent manner similar to its inhibition of FDM when administered via intravitreal injections or topical eye drops. In both FDM and LIM, levodopa injections remained protective against myopia when co-administered with SCH-23390, but not spiperone, indicating that levodopa elicits its protection through a dopamine D2-like receptor mechanism in both paradigms.
Highlights
Animal models have demonstrated a link between dysregulation of the retinal dopamine system and the development of myopia
Number of animals 8 8 7 8 8 6 6 6 6 8 6. These findings suggest that a depletion in retinal dopamine release is associated with myopic eye growth. In accordance with this hypothesis, we have previously shown in chicks that topical or intravitreal application of the dopamine precursor, levodopa, can increase retinal dopamine release and inhibit the development of form-deprivation myopia (FDM) in a dose-dependent m anner[27]
To expand on our previous work in FDM, we investigate here whether this same dose-dependent protection can be generated in chicks undergoing lens-induced myopia (LIM), as the role of dopamine in this experimental model is less clear[36,37,38]
Summary
Animal models have demonstrated a link between dysregulation of the retinal dopamine system and the development of myopia (short-sightedness). The protective effects of brief periods of normal vision against the development of FDM in chicks is lost by modulating dopaminergic function by either keeping the animals in the dark during diffuser removal, inhibiting dopamine release, or by injecting a dopaminergic D2-like receptor a ntagonist[19] Together, these findings suggest that a depletion in retinal dopamine release is associated with myopic eye growth. These findings suggest that a depletion in retinal dopamine release is associated with myopic eye growth In accordance with this hypothesis, we have previously shown in chicks that topical or intravitreal application of the dopamine precursor, levodopa, can increase retinal dopamine release and inhibit the development of FDM in a dose-dependent m anner[27]. This is referred to as a closed-loop system as there is a defined endpoint, with eye growth returning to normal growth rates once compensation to the imposed defocus is achieved
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