Retinal ischemia can be effectively modeled by permanent bilateral common carotid
artery occlusion, which leads to chronic hypoperfusion-induced degeneration in the
entire rat retina. The complex pathways leading to retinal cell death offer a complex
approach of neuroprotective strategies. In the present review we summarize recent
findings with different neuroprotective candidate molecules. We describe the protective
effects of intravitreal treatment with: (i) urocortin 2; (ii) a mitochondrial ATP-sensitive
K(+) channel opener, diazoxide; (iii) a neurotrophic factor, pituitary adenylate cyclase
activating polypeptide; and (iv) a novel poly(ADP-ribose) polymerase inhibitor (HO3089).
The retinoprotective effects are demonstrated with morphological description and effects
on apoptotic pathways using molecular biological techniques.