Objective To observe changes in retinal functions, structure, and glutamate content after retinal ischemia-reperfusion(RIR)injury in Long Evans rats to provide a reference for the study of retinal injury and possible protective mechanisms. Methods Thirty adult SPF level Long Evans rats were randomly selected, and the left anterior chamber of their left eye was perfused with high-pressure normal saline for 60 minutes to establish an RIR injury model, while the right eye was untreated as a control. At 1, 3, 7, and 14 days after modeling, changes in retinal electrophysiological functions were assessed by flash electroretinogram. The retinal thickness was measured by optical coherence tomography(OCT)before and at 3, 7 and 14 days after modeling. Changes in fundus vessels were observed by fundus angiography. Rats were sacrificed at 14 days after modeling, and the retinal morphology, apoptosis, and distribution were observed by hematoxylin-eosin(HE) and TdT-mediated dUTP nick end labeling(TUNEL) staining. The content of glutamate in the retina was detected by ELISA. Results Compared with control eyes, the B wave amplitude of the electroretinogram in the model eyes were decreased significantly(P<0. 01)and latency was delayed significantly(P<0. 01) from the first day. OCT showed that the thickness of the retinal ganglion cell complex(GCC)was significantly thinner from day 3(P<0. 01), the thickness of the whole retina was significantly thinner from day 7(P<0. 01), and both of them became thinner over time(P<0. 05). Fundus images showed that the retina had obvious ischemia from day 3 and did not recover to the normal level until day 14. On day 14, the HE staining showed retinal atrophy, obvious thinning of the inner layer and a reduction of retinal ganglion cells. TUNEL staining showed obvious apoptosis in all retinal layers. ELISAs showed that the glutamic acid content in the retina was increased after modeling(P<0. 05). Conclusions RIR injury in Long Evans rat causes serious damage to visual electrophysiological functions, retinal atrophy, an obvious reduction in the GCC thickness over time that becomes irreversible, RGC apoptosis, fundus vascular ischemia, and an increased retinal glutamate content, thereby providing a good animal model to study retinal injury diseases.