We investigated the expression and cellular localization of growth-associated protein (GAP)-43 in the rat retina following ischemia induced by transiently increased intraocular pressure. In the normal retina, GAP-43 immunoreactivity was restricted to profiles in the inner plexiform layer. Following ischemia and reperfusion, immunoreactivity appeared in ganglion cells. The cell density of labeled ganglion cells peaked three days post-lesion and then decreased at seven days. Quantitative evaluation by immunoblotting confirmed that GAP-43 expression increased at three days (to 190% of control levels) and then slightly decreased at seven days. Our findings suggest that some ganglion cells have the potential to regenerate through the up-regulation of GAP-43 in the ischemic rat retina.