Early Photoreceptor Apoptosis and Microglial Response in Light-Damaged Mouse Retina

Abstract

Background: The retina, as part of the central nervous system, has limited capacity for self-repair following injury. Light-induced retinopathy serves as a valuable model for studying retinal degeneration, but the early events following photic injury remain incompletely characterized.

Objective: This study investigated the temporal and spatial relationship between photoreceptor apoptosis and macrophage response during the first three days after light-induced retinal damage.

Methods: Adult BALB/c mice were exposed to intense cool white fluorescent light (3,500-7,000 lux) for 7 hours and sacrificed at 1, 2, and 3 days post-injury. Retinal sections were examined using toluidine blue staining for morphology, TUNEL assay for apoptotic cells, and F4/80 immunohistochemistry for macrophages/microglia.

Results: Progressive outer nuclear layer (ONL) thinning was observed, with near-complete photoreceptor loss by day three. TUNEL-positive apoptotic cells appeared exclusively in the ONL, peaking at day two and declining by day three. F4/80-positive cells transformed from ramified to amoeboid morphology, increased in number, and migrated to the ONL, with peak accumulation at days two to three.

Conclusion: Photoreceptor apoptosis peaks at 48 hours post-injury, closely followed by microglial activation and recruitment to the site of damage. This temporal sequence confirms a direct relationship between cell death and inflammatory response, identifying the first 48 hours as a critical therapeutic window for intervention in retinal degenerative diseases.