This study examined anatomical and genetic factors behind retinal photic injury (RPI) severity in rats (WKY, LEW parental strains, F1, and backcross generations; total n=77 for morphometry, n=34 BC4 for genotyping), using geodesic length morphometry to map lesion extent in sagittal sections and correlating findings with Morris water maze (MWM) spatial navigation performance.
RPI lesions centered 2.15 mm superior to the optic nerve head; a critical inferior boundary at 1.95 mm below the ONH predicted MWM impairment (swimming time ≥10 s), while lesions not crossing 0.98 mm inferior to the ONH left navigation intact. The WKY-derived Rpi1 locus strongly controlled whether degeneration surpassed these thresholds, yielding a triphasic severity classification.
Findings are in an animal model (rat) and may not directly translate to human retinal disease; the total morphometric sample is modest (n=77); genotypic analysis was limited to BC4 backcross individuals (n=34), leaving the precise gene(s) at the Rpi1 locus unidentified.
This work is preclinical and not directly actionable in clinical practice, but it defines precise anatomical thresholds for functional vision loss after light-induced retinal injury, which could inform future translational work on retinal degeneration susceptibility.
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