Abstract

To investigate the effects of visible light on the retinal development, we established an early-light-exposure model in neonatal mice. An incision was made on the right-sided eyelids of mice on postnatal day 4 (P4), and so that the right eyes were exposed to visible light (4000 lux) for 12h per day. The population in the retinal ganglion cells (RGCs), cellular apoptosis and lumican expression were analyzed in the retinae. The loss of the RGCs was moderately alleviated and dramatically increased by early light exposure on P9 and P12, respectively. In the light-exposed retinae, the immunoactivities of caspase-9 (p39), an active isoform of caspase-9 marking the cellular apoptosis, dropped to nearly 30% of those in the control specimens on P6; thereafter the light-induced lower levels of caspase-9 (p39) remained, while those in the control specimens dropped to the values less than 50% of the light-exposed retinae. Lumican was first ectopically detected on P9, and distributed in the inner layers of the light-exposed retinae, with the most significant accumulation in the ganglion cell layer by P12. The ectopic expression of lumican was both temporarily and spatially parallel with the aggravated loss of the RGCs. In conclusion, early light exposure inflicts a profound effect on the immature retina. Our studies may have implications for premature infant care.

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