To determine whether the localization of retinal glutamate transporters is affected by retinal ischaemia and whether their ability to transport glutamate decreases with the progression of ischemic retinal and optic nerve degeneration.Retinal ischemia was induced in rats by acutely increasing the intraocular pressure (IOP, 110 mmHg/60 min). Reperfusion was permitted for periods up to 60 days post-ischemia. Functional evaluation was performed by monitoring the pupil light reflexes (PLRs) and electroretinograms (flash, flicker ERG and oscillatory potentials). Glutamate transporter localization and d-aspartate (glutamate analogue) uptake were assessed by immunohistochemistry. Intense immunoreactivity for the retinal glutamate transporters (GLAST, GLT1, EAAC1 and EAAT5) was observed at all time points after the insult, despite severe retinal degeneration. d-aspartate was also normally accumulated in the ischemic retinas. Ten days post-operatively the PLR ratio (ratio=indirect/direct PLR=34±7·5%) was significantly less than the pre-operative value (pre-op=76·7±2·6%, p<0·05). However, 25 and 35 days post-operatively PLR ratios did not differ significantly from pre-operative values (44·4±6·9 and 53·8±9·6%, p>0·05). Forty-five and 60 days post-operatively the PLR ratio declined again and was significantly lower than the pre-operative value (33·8+8·7 and 26·2+8·9%, p<0·05). Statistical analysis revealed that all tested ERG components had significantly higher values at 32, but not at 42 and 58 days post-operatively when compared to the first time point recorded post-operatively (10 days).While retinal glutamate transport is compromised during an acute ischemic insult, consequent retinal recovery and degeneration are not due to a change in the excitatory amino acid transporter localization or d-aspartate (glutamate analogue) uptake. Rat retina and optic nerve are capable of spontaneous, but temporary, functional recovery after an acute ischemic insult.