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Harry Zwick, Bruce Stuck, Peter Edsall, Ed Wood, Rachel Cheramie, Jim Sankovich; In Vivo characterization of laser induced photoreceptor damage and recovery in the high numerical aperture of the snake eye. Journal of Vision 2005;5(8):302. doi: 10.1167/5.8.302.
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© ARVO (1962-2015); The Authors (2016-present)
The high numerical aperature of the garter snake eye (Thamnophis m. Marcianus) permits in vivo imaging of the photoreceptor layer and anterior retinal blood cell activity. A Rodenstock confocal scanning laser ophthalmoscope (CSLO) was employed with laser imaging sources at 488, 514.5, 633, and 790 nm. Photoreceptor damage was examined for both thermal/mechanical as well as non-thermal/mechanical photoreceptor damage mechanisms. Anesthesia was induced with ketamine-xylezine, IM. Acute thermal/mechanical laser induced photoreceptor injury from external laser sources causes visible photoreceptor damage, characterized by high reflectivity in photoreceptors at the edge of the lesion site and loss of photoreceptors at the lesion center. During the first 60 seconds post exposure, photoreceptors may migrate in various directions away from the lesion site and individual photoreceptor orientations maybe altered. Utilization of the 790 nm CSLO imaging source revealed maximal in vivo photoreceptor reflectivity as compared with shorter wavelengths (488 nm), as longer wavelength imaging sources focus within the altered outer segment lamellae, while shorter wavelength sources focus closer to the posterior edge of the photoreceptor outer segment. Examining comparable exposure conditions at the level of the retinal vasculature reveals the appearance of “sticky” blood cells which cumulate in the retinal photoreceptor and retinal nerve fiber layer (RNFL) injury sites and have been identified with acridine orange as leukocytes. At non-thermal levels of exposure, photoreceptors undergoing oxidative stress have been identified with H2DCFD,D-399,adjacent to photoreceptors injured under thermal mechanical conditions. Long term evaluation of photoreceptor damage sites show a decrease in photoreceptor lesion site size, suggesting photoreceptor reorganization and replacement and raises the issue that such migration might be driven by active as well as passive photoreceptor recovery mechanisms.
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