Abstract:

Purpose: To determine whether bright light (BL) inhibits form deprivation myopia (FDM) via the dopamine receptor D1 (D1R)-linked  signaling pathway localized in specific retinal neuronal cell types in mice.
Methods: D1R antagonist SCH39166 was daily intraperitoneally injected to evaluate if BL mediates declines in FDM development through D1R. Refraction changes were evaluated with an eccentric infrared photorefractor. Optical coherence tomography evaluated ocular axial components. Electroretinography monitored retinal function. c-Fos and p-TH (phosphorylated tyrosine hydroxylase) immunofluorescent staining evaluated D1R receptor activity and dopamine synthesis, respectively. Six different biomarkers of retinal neuronal types delineated di?erential distribution of D1R expression.
Results: BL (2500-5000 lux) exposure for 4 weeks (6 hours per day) inhibited FDM development by reducing ocular elongation and shifting refraction towards hyperopia compared to that in normal light (NL, 100-200 lux ). SCH39166 injections completely reversed the inhibitory effects of BL on both refraction and ocular elongation. BL increased the number of cells expressing p-TH and c-fos expression in D1R+ BCs, especially in D1R+ON-BCs as well as horizontal cells (HCs).
Conclusions: BL increases D1R activity in the bipolar cells (BC) of the ON pathway and HCs, which is associated with less myopic shift and ocular elongation than that occurring in NL. This di?erence suggests that BL-induced increase in the activity of D1R in the ON pathway contributes to the suppression of FDM development in mice.

Key words: Form-deprivation myopia, Bright light, Dopamine, Dopamine D1 receptor, ON-bipolar cells, OFF-bipolar cells, c-fos