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In adult Sprague-Dawley rats, retinal ganglion cell survival was investigated after intraorbital optic nerve section and after transient ischemia of the retina induced by elevation of the intraocular pressure or by selective ligature of the ophthalmic vessels. The thickness of the inner nuclear and inner plexiform layers was also assessed after transient periods (120 min) of retinal ischemia induced by selective ligature of the ophthalmic vessels. In addition, we have also investigated the neuroprotective effects of different substances in these paradigms. The intraocular injection of brain-derived neurotrophic factor increased RGC survival after retinal ischemia induced by elevation of the intraocular pressure or by selective ligature of the ophthalmic vessels. The caspase-inhibitor Z-DEVD increased retinal ganglion cell survival after optic nerve section and also after 90 min of retinal ischemia induced by selective ligature of the ophthalmic vessels. The peptide Bcl-2 did not increase retinal ganglion cell survival after optic nerve section but increased retinal ganglion cell survival after 60 or 90 min of retinal ischemia induced by selective ligature of the ophthalmic vessels. Finally, BDNF, nifedipine, naloxone and bcl-2 prevented in part the decrease in thickness of the inner nuclear layer and inner plexiform layer induced by selective ligature of the ophthalmic vessels. Our results suggest that retinal ganglion cell loss induced by different types of injury, may be prevented by substances with neuroprotective effects, by altering steps of the cascade of events leading to cell death.

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Purpose Brimonidine is a lowering pressure agent currently used in glaucoma. This chronic degenerative condition is characterised by neuronal death, and an agent which offers neuroprotection may slow down or impede the progression of neuronal cell death. Methods The effects of brimonidine (BMD) on the short- and long-term survival of retinal ganglion cells (RGCs) after transient retinal ischaemia are reported here using a rat model. The fluorescent tracer Fluorogold (FG) was applied to both superior colliculi to retrogradely label RGCs. A ninety-minute period of ischaemia was induced and densities of surviving RGCs were estimated over time by counting FG-labelled RGCs in 12 standard regions of each retina. Results Seven days after inducing transient ischaemia, there was loss of approximately half of the RGC population. Topical pre-treatment with 0.1% or 0.5% BMD prevented ischaemia-induced RGC death. Conclusions These results indicate that optimal neuroprotective effects against the early loss of RGCs are seen with 0.1% or 0.5% BMD. Ischaemia-induced RGC loss continued between day 7 and day 21 in the vehicle treated groups and amounted to approximately 25% of the RGC population. Topical pre-treatment with 0.1% or 0.5% BMD was also effective in reducing the slow loss of RGCs.

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