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.
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.