We investigated the post-ischemic change in [3H]L-
N(G)-nitroarginine binding as a marker of
nitric oxide (
NO) synthase in the animal brain after transient global
ischemia or transient focal
ischemia. Transient global
ischemia in gerbils was induced for 10 min followed by 1 h to 7 days of recirculation. Transient focal
ischemia in rats was induced for 45 min followed by 3 days of recirculation. Following transient global
ischemia, [3H]L-
N(G)-nitroarginine binding showed a significant increase in the striatum (17-18%) and hippocampal CA1 sector (24%) at 48 and 24 h after recirculation, respectively. The hippocampal CA3 sector also showed a significant elevation (32-40%) in [3H]L-
N(G)-nitroarginine binding at 24 and 48 h after global
ischemia. Furthermore, the dentate gyrus showed a significant increase (30-32%) in [3H]L-
N(G)-nitroarginine binding at 5, 24 and 48 h after global
ischemia. Thereafter, a significant reduction in [3H]L-
N(G)-nitroarginine binding was observed only in the dentate gyrus 7 days after recirculation. In contrast, [3H]L-
N(G)-nitroarginine binding was unchanged in the thalamus throughout the recirculation periods. Histological analysis revealed that transient global
ischemia caused severe damage or cellular damage in the striatum and the hippocampal CA1 sector. The hippocampal CA3 sector and thalamus were mildly damaged, whereas the dentate gyrus was morphologically intact. Following transient focal
ischemia, a marked elevation (50-52%) in [3H]L-
N(G)-nitroarginine binding was found in the regions of the ipsilateral striatum in which severe
infarction occurred. Our findings suggest that [3H]L-
N(G)-nitroarginine binding increases in the striatum and hippocampus after transient global
ischemia or transient focal
ischemia. This increase in [3H]L-
N(G)-nitroarginine binding may play a pivotal role not only in the pathogenesis of ischemic brain damage, but also in the restoration of injury areas after
cerebral ischemia.