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M Villegas-Perez, M Avilés-Trigueros, MP Lafuente, ME Rodríguez, A Garcia-Avilés, L Coll, S Mayor-Torroglosa, J Miralles de Imperial, M Vidal-Sanz; Axonal Transport Preservation in Adult Rat Retinal Ganglion Cells Protected From Ischemia Induced Cell Death by Brimonidine . Invest. Ophthalmol. Vis. Sci. 2002;43(13):764.
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Purpose: In previous studies, we have shown that topically-administered brimonidine (BMD) protects retinal ganglion cells (RGCs) from ischemia induced cell death. Here we investigate if these cells retain their retrograde and orthograde axoplasmic transport. Methods: In adult Sprague-Dawley rats, transient ischemia of the left retina was induced by ligature of the ophthalmic vessels (LOV) for 90 minutes. One hour befores ischemia the left eye was treated with two 5 µl drops of saline alone (vehicle-treated group), or saline containing 0.5% BMD (BMD-treated group). Retrograde axonal transport was investigated at 7 or 14 days after ischemia by estimating, in both ischemic and contralateral non-ischemic retinas, the densities of RGCs labelled with Fluorogold (FG) that had been applied to both superior colliculi (SC) 1 hour or 7 days, respectively, after LOV. Anterograde axonal transport was investigated 30 or 60 days after LOV by injecting, 5 days before sacrifice, the tracer cholera toxin subunit b (CTB) in the vitreous of the left eye. Serial coronal sections of the midbrain were immuno-stained for CTB and the extension of areas densely innervated by CTB-labelled RGC terminals in the visual layers of the contralateral SC was determined with the aid of an image analysis system. Results: Retrograde transport; in the vehicle treated rats, 7 or 14 days after LOV, the densities of FG-labelled RGCs in the left retinas had diminished to 40 or 27%, respectively, of their contralateral non-ischemic retinas. The BMD treated rats showed 7 or 14 days after LOV, densities of FG-labelled RGCs in their left retinas that were comparable to those found in their right control non-ischemic retinas. Anterograde transport; the vehicle treated rats showed areas devoid of CTB-labelled RGC terminals in the visual layers of the contralateral SC. These areas were larger and more numerous 60 days after LOV than 30 days after LOV. The BMD treated rats showed 30 and 60 days after LOV a qualitative normal density of CTB-labelled RGC terminals spanning the entire visual layers of the contralateral SC. Conclusion: RGCs protected from ischemia-induced cell death by brimonidine also retain their retrograde and orthograde axoplasmic transport long periods of time after injury.
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