Axotomy-induced retinal ganglion cell death in development: its timecourse and its diminution by antioxidants

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Abstract
Developing neurons die when deprived of trophic support from their axonal target. Although this is generally attributed to the programmed expression of suicide proteins, recent data suggest that a less orderly mechanism involving oxidative stress may also be involved. We have studied retinal ganglion cell death in the chick embryo after a contralateral tectal lesion. The kinetics of cell death, as judged from counts of pyknotic cells, are described. In addition, we show that the pyknotic counts are reduced following intraocular injections of the protein synthesis inhibitor cycloheximide or the antioxidants N-t-butyl-$\alpha $-phenylnitrone and N-acetyl cysteine. Our results suggest that target deprivation-induced ganglion cell death involves oxidative stress.