Post-ischaemic alteration of excitatory amino acid transport sites in the gerbil hippocampus

Sodium-dependent [H-3]D-aspartate binding as a marker of excitatory amino acid transport sites in the gerbil hippocampus was evaluated by quantitative receptor autoradiography 1 h to 7 days after transient cerebral ischaemia for 10 min. Sodium-dependent [H-3]D-aspartate binding in the hippocampal CA1 and CA3 sectors significantly increased in the early post-ischaemic stage. After 7 days, a conspicuous elevation of sodium-dependent [H-3]D-aspartate binding was observed in the hippocampal CA1 sector and dentate gyrus. However, no significant change in the binding was found in the hippocampal CA3 sector. A histological study revealed that transient ischaemia caused severe neuronal damage in the hippocampal CA1 sector and mild damage in the hippocampal CA3 sector. However, no ischaemic neuronal damage was observed in the dentate gyrus. An immunohistochemical study also showed that numerous reactive astrocytes were evident in the hippocampus, particularly in the hippocampal CA1 sector, 7 days after ischaemia. These results demonstrate that transient cerebral ischaemia can cause marked elevation in excitatory aminoacid transport sites in the hippocampus. Furthermore, our results suggest that the post-ischaemic increase in excitatory amino acid transport sites might reflect expression of reactive astrocytes. These findings are of interest in relation to the mechanisms of ischaemic hippocampal damage.