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Ruth Estela Rosenstein, Maria F Gonzalez Fleitas, Marcos L Aranda, Nuria de Zavalia, Pablo Sande, Damian Dorfman; Retinal Ganglion Cells Expressing Melanopsin Are Injury-Resistant After Retinal Ischemia.. Invest. Ophthalmol. Vis. Sci. 2014;55(13):1895.
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We investigated the effect of acute retinal ischemia on the non-image forming visual system, particularly on melanopsin expressing retinal ganglion cells (RGC).
Ischemia was induced in male Wistar rats by increasing intraocular pressure (120 mm Hg for 40 min). Retinal function (ERG), the number of Brn3a(+) and melanopsin(+) RGC (immunohistochemistry), and melanopsin levels (Western Blot), as well as the pupil light reflex (PRL) (after 30-s light flash) were examined. Anterograde transport was examined after an intravitreal injection of cholera toxin β-subunit, and circadian rhythms of general locomotor activity were registered in cages equipped with infrared detectors of motion.
After 4 weeks of ischemia, clear alterations in the visual function and retinal histology were observed. Concomitantly with a significant decrease in the number of Brn3a(+) RGC, no differences in the number of melanopsin(+) cells, and melanopsin levels were observed between non-ischemic and ischemic retinas. Ischemia decreased retinal projections to the superior colliculus, whereas the anterograde transport to the suprachiasmatic nucleus and the olivary pretectal nucleus remained unaffected. No differences in PRL were observed between control and ischemic eyes, and the locomotor activity pattern was conserved in animals submitted to bilateral ischemia.
These results indicate melanopsin(+) RGC, and the non-image forming visual system are resistant to ischemic injury.
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