Araki T, Kanai Y, Murakami F, Kato H, Kogure K
Department of Neurology, Tohoku University School of Medicine, Sendai, Japan.
Pharmacol Biochem Behav. 1993 Aug;45(4):945-9. doi: 10.1016/0091-3057(93)90145-j.
We performed receptor autoradiography to determine sequential changes in the binding of N-methyl-D-aspartate (NMDA) and gamma-aminobutyric acidA (GABAA) 1 h to 1 month after 10 min of transient cerebral ischemia in the gerbil. [3H]MK-801 and [3H]muscimol were used to label NMDA and GABAA receptors, respectively. [3H]MK-801 binding showed no significant changes in the striatum and hippocampus at an early stage (1-24 h) after ischemia. Thereafter, [3H]MK-801 binding exhibited a significant reduction in the dorsolateral striatum, most of hippocampal CA1 sector and dentate gyrus 48 h or 7 days of recirculation. However, [3H]MK-801 binding progressively depressed in the hippocampal CA1 sector 1 month after ischemia, whereas other regions showed no significant alteration in the binding. By contrast, [3H]muscimol binding was unchanged in all brain areas throughout the recirculation period. A histological study also demonstrated that transient ischemia caused severe neuronal damage in the striatum and hippocampus. These results demonstrate that NMDA and GABAA receptors are relatively resistant to severe degenerative processes. Furthermore, our finding suggests that transient ischemia may induce long-term changes in the properties of survival neurons or interneurons especially in the hippocampal CA1 sector.