We investigated the distribution and expression of glutamate-binding protein (GBP) in the rat retinas after ischemia-reperfusion injury. Ischemia-reperfusion injury was induced in rats by clamping of the optic nerve for one hour. The distribution of GBP immunoreactivity was determined at 6, 24, 72, and 168 hours after reperfusion. Also, RT-PCR was performed to detect the change of GBP mRNA expression in the reperfused retinas. In untreated control retinas, GBP immunoreactivity was observed in the cells of ganglion cell layer, inner plexiform layer, and inner nuclear layer. At 6, 24, and 72 hours after reperfusion, GBP immunoreactivity was seen not only in the GCL, IPL, and INL, but also in the outer plexiform layer and photoreceptor outer segment. At 168 hours after reperfusion, GBP immunoreactivity in the OPL was decreased. Moreover, we found increased GBP mRNA expression at 24 hours after reperfusion. In this study, we demonstrated that ischemia-reperfusion induced increase of GBP immunoreactivity in the inner retina and increase of GBP mRNA expression in the rat retinas. Our results suggest that NMDA receptor-like complex may play some role in the ischemic cell death of the inner retina.