γ-Aminobutyric acid (GABA) is normally primarily in amacrine cells in the rat retina. Immediately after an ischaemic insult, attained by occlusion of the central retinal artery for 60 min, GABA is then found to be associated with Müller cells. During subsequent reperfusion, the distribution of GABA immunoreactivity gradually reverts from the glial cells back into neuronal elements of the retina. Twenty-four hours after ischaemia, GABA staining is indistinguishable from that seen in control animals. It is suggested that during central retinal artery occlusion, Müller cell energy levels are sufficient to allow the active uptake of released GABA, but insufficient to metabolise it to glutamine. The normal cycle of GABA metabolites from Müller cells to neurones is thus inhibited. Restoration of blood flow and the consequent in retinal energy levels, as indicated by a slight recovery of the electroretinogram b-wave, facilitates glutamine shunting between glial cells and amacrine cells, resulting in the synthesis of neuronal GABA.