Effects of vinconate and pentobarbital against postischemic alterations in spirodecanone binding sites in the gerbil brain.
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.
Murakami
F
F
Pharmacological Research Laboratory, Tokyo Tanabe Co. Ltd., Japan.
Araki
T
T
Kanai
Y
Y
Kato
H
H
Fujiwara
T
T
Kogure
K
K
D000818:Animals; D001345:Autoradiography; D001665:Binding Sites / Q000187:drug effects; D003342:Corpus Striatum / Q000187:drug effects* / Q000473:pathology; D005849:Gerbillinae; D005904:Glial Fibrillary Acidic Protein / Q000276:immunology; D006624:Hippocampus / Q000187:drug effects* / Q000473:pathology; D002546:Ischemic Attack, Transient / Q000188:drug therapy* / Q000473:pathology; D008297:Male; D010424:Pentobarbital / Q000627:therapeutic use*; D011954:Receptors, Dopamine / Q000032:analysis*; D013141:Spiro Compounds / Q000032:analysis; D014748:Vinca Alkaloids / Q000627:therapeutic use*
D005904:Glial Fibrillary Acidic Protein; D011954:Receptors, Dopamine; D013141:Spiro Compounds; D014748:Vinca Alkaloids; C038349:spirodecanone receptor; C014826:spirodecanone; C038627:vinconate; D010424:Pentobarbital