We investigated the effects of
vinconate and
pentobarbital against the alterations in
spirodecanone binding in the gerbil striatum and hippocampus 5 h and 7 days after 10 min of
cerebral ischemia, using receptor autoradiography.
Vinconate and
pentobarbital were given intraperitoneally 10 and 30 min prior to ischemic insult, respectively. The
spirodecanone binding in vehicle-treated gerbils subjected to
ischemia was unchanged in the brain 5 h after recirculation, compared with that in
sham-operated animals. Seven days after
ischemia, a significant elevation in the
spirodecanone binding was observed in the striatum and the stratum radiatum of the hippocampal CA1 sector and the hippocampal CA3 sector of the vehicle-treated animals. Other regions showed no significant change in the binding.
Vinconate and
pentobarbital showed no significant change in the striatum and hippocampus 5 h after
ischemia. However, the administration of
vinconate inhibited a significant elevation in the
spirodecanone binding in the lateral striatum and the stratum radiatum of hippocampal CA1 sector 7 days after
ischemia.
Pentobarbital also prevented a significant elevation only in the lateral striatum. A histological study revealed that
cerebral ischemia caused severe neuronal damage in the lateral striatum and hippocampal CA1 and CA3 sectors. However, ischemic neuronal damage was not 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
ischemia. The present study demonstrates that
cerebral ischemia can cause a conspicuous elevation in
spirodecanone binding in the striatum and hippocampus. They also suggest that the postischemic elevation in the
spirodecanone binding is partly prevented by treatment with
vinconate and
pentobarbital. These results suggest that the postischemic elevation in
spirodecanone binding sites may reflect expression of reactive astrocytes.