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P72 We have previously demonstrated that the delayed cell death  that occurs in the inner retina following transient global ischemia is  in part apoptotic.In non-neuronal cells, death-inducing ligands(DILs)  such as TNF-α and FasL are important in the induction of  apoptosis.The purpose of this study was to investigate the role of DILs  in the selective vulnerability of the inner retina to ischemic injury.  Four groups of mice were subjected to transient global retinal ischemia  (high intraocular pressure model) for a period of 45 minutes : wild  type, TNFR(p55)-knock out, TNFR(p75)-knock out and lpr(loss of function  of Fas receptor). The degree of retinal damage was assessed by  measuring the thicknesses of the inner retinal layers. Additionally,  electrophysiology (ERG) was performed following ischemia to assess  functional outcome. There were TUNEL positive cells within the  vulnerable inner retina seen maximally at 24 hours following ischemia.  At 7 days subsequent to ischemia,in all groups of mice there was marked  thinning of the inner retinal layers with morphological characterstics  of apoptosis. ERG at 7 days demonstrated diminished amplitude of the  ERG-b wave.In all three groups of mutant mice, there was significantly  less morphological damage(mean inner retinal thickness) as well as  significant preservation of the ERG-b wave as compared to the wild type  animals.The lpr animals demonstrated the greatest protection.These data  suggest that DILs play a critical role in the selective vulnerability  of the inner retina to transient global ischemia and offer new  strategies for the treatment of ischemic neuronal injury.

Death inducing ligands are critical for the selective vulnerability of the inner retina to transient global ischemia.