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M. Vidal-Sanz, M.P. Lafuente, S. Mayor, M.E. Aguilera, J. Miralles de Imperial, M.P. Villegas-Pérez; Transient Ischemia of the Retina Results in Altered Retrograde Axonal Transport by Retinal Ganglion Cells: Neuroprotection With Brimonidine . Invest. Ophthalmol. Vis. Sci. 2003;44(13):5215.
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Purpose: To investigate the effects of transient ligature of the ophthalmic vessels (LOV) and administration of brimonidine (BMD) on retinal ganglion cells (RGCs) retrograde axonal transport. Methods: Adult Sprague-Dawley rats received in their left eyes, 1 hour prior to ischemia, two 5 µl drops of saline or 0.5% brimonidine (BMD). Retinal ischemia was induced by transient ligature of the left ophthalmic vessels for 90 minutes. FG (FG) was applied to both superior colliculi 1 week before LOV, or 1 hour or 1 week after LOV. Animals were processed 1 or 2 weeks after LOV and RGC densities were estimated in the right control and left experimental retinas. In an additional group the regrograde tracer DiI was applied to both SCi three weeks before LOV, FG was applied to the intraorbitally cut optic 9 nerve days after LOV and animals were analysed 2 weeks after ischemia. Results: Seven days after LOV the densities of FG-labelled RGCs in the ischemic retinas had diminished to 53% or 39% of their contralateral non-ischemic retinas, in the animals in which FG was applied to the SC 7 days before LOV or 1 hour after LOV, respectively. Fourteen days after LOV, the densities of FG-labelled RGCs in the ischemic retinas had diminished to 48% or 27% of their contralateral non-ischemic retinas, in the animals in which FG was applied to the SC 7 days before LOV or 7 days after LOV, respectively, thus suggesting that some of the RGCs surviving LOV have their retrograde axonal transport impaired. Fourteen days after LOV, the densities of FG-labelled RGCs were smaller than those DiI-labelled, and approximately 33,5% of the DiI-labelled RGCs were also doubly labelled with FG, a proportion significantly smaller than that found in control rats, thus confirming that retinal ischemia induces, in addition to RGC death, an altered retrograde axonal transport in a proportion of surviving RGCs. In the left retinas of the BMD pre-treated animals, RGC densities amounted to 90% of the RGC population 7 or 14 days after ischemia and were comparable to those obtained in their contralateral non-ischemic retinas. Conclusions: Retinal ischemia results in impaired retrograde axonal transport in a proportion of surviving RGCs. Topical pre-treatment with BMD not only prevents the loss of ischemia-injured RGCs but also preserves retrograde axonal transport in these cells
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