['The glaucomas are characterized by chronic progressive ganglion cell loss over many years. A drug with neuroprotective activity should increase the resistance of retinal ganglion cells (RGC) to chronic stress or injury and therefore enhance survival. Brimonidine is a highly selective and potent alpha-2 adrenergic receptor agonist, which lowers intra-ocular pressure (IOP) and is neuroprotective. Immunohistochemistry data have shown that the specific receptor targets, the alpha-2 receptors, are located in the inner retina.', 'Brimonidine 0.1 mg/kg given intraperitoneally promoted RGC survival compared with vehicle using the optic nerve crush model even when administered up to 24 hours before injury. Using the chronic ocular hypertensive rat model, brimonidine 1 mg/kg/day (with osmotic pump) significantly prevented the loss of RGCs when compared with vehicle or timolol. This ability was due to the neuroprotective action of brimonidine, since it did not affect IOP. In addition, brimonidine 0.1 mg/day reached concentrations in the retina of Sprague-Dawley rats within 30 minutes of injection, which was sufficient to activate the alpha-2 receptor (> or = 2 nM) and maintained these concentrations for 6 hours.'] Are alpha-2 adrenergic receptor agonists neuroprotective in experimental models of glaucoma?