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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2004-7-21
pubmed:abstractText
We investigated postischemic alterations in benzodiazepine receptor, D1 dopamine receptor, and muscarinic acetylcholine receptor binding after transient middle cerebral artery (MCA) occlusion in rats using [3H]-flumazenil, [3H]-SCH23390, and [3H]-N-methyl-4-piperidyl benzilate ([3H]-NMPB), respectively, as radioligand. These ligand bindings were determined at 3 and 24 h and at 3 and 7 days after ischemia/reperfusion of MCA by using autoradiographic methods. Ischemic cell injury was clearly detected from 3 h after ischemia/reperfusion and progressively increased from 3-24 h after ischemia/reperfusion of MCA. The area of cell injury reached maximum at 24 h after ischemia/reperfusion of MCA. [3H]-SCH23390 binding was reduced to 47% of the contralateral side at 3 days after ischemia/reperfusion of MCA. After 7 days, [3H]-SCH23390 binding was further reduced by 20% in the striatum. [3H]-NMPB binding was slightly decreased in both the striatum and cerebral cortex at 3 days after ischemia/reperfusion of MCA, and [3H]-NMPB binding in the striatum and cerebral cortex were reduced to 42 and 62% of the contralateral side at 7 days after ischemia/reperfusion of MCA. [3H]-NMPB was also decreased at 24 h. In contrast, [3H]-flumazenil binding was not decreased in the striatum and cerebral cortex within 7 days after ischemia/reperfusion of MCA. These results suggest that [3H]-SCH23390 and [3H]-NMPB binding do not correlate with cell injury by ischemia/reperfusion, although vulnerability to ischemia/reperfusion was observed with these receptors. In addition, central benzodiazepine receptor imaging might be essentially stable to neuronal cell injury induced by transient focal cerebral ischemia in rats, in contrast to the results of PET studies.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0887-4476
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
53
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
234-9
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:15266555-Animals, pubmed-meshheading:15266555-Autoradiography, pubmed-meshheading:15266555-Benzazepines, pubmed-meshheading:15266555-Benzilates, pubmed-meshheading:15266555-Binding, Competitive, pubmed-meshheading:15266555-Binding Sites, pubmed-meshheading:15266555-Cerebral Cortex, pubmed-meshheading:15266555-Cerebral Infarction, pubmed-meshheading:15266555-Corpus Striatum, pubmed-meshheading:15266555-Disease Models, Animal, pubmed-meshheading:15266555-Down-Regulation, pubmed-meshheading:15266555-Flumazenil, pubmed-meshheading:15266555-Infarction, Middle Cerebral Artery, pubmed-meshheading:15266555-Male, pubmed-meshheading:15266555-Nerve Degeneration, pubmed-meshheading:15266555-Piperidines, pubmed-meshheading:15266555-Radioligand Assay, pubmed-meshheading:15266555-Rats, pubmed-meshheading:15266555-Rats, Wistar, pubmed-meshheading:15266555-Reaction Time, pubmed-meshheading:15266555-Receptors, Dopamine D1, pubmed-meshheading:15266555-Receptors, GABA-A, pubmed-meshheading:15266555-Receptors, Muscarinic, pubmed-meshheading:15266555-Reperfusion Injury, pubmed-meshheading:15266555-Sensitivity and Specificity, pubmed-meshheading:15266555-Tritium
pubmed:year
2004
pubmed:articleTitle
Discrepancy between cell injury and benzodiazepine receptor binding after transient middle cerebral artery occlusion in rats.
pubmed:affiliation
Department of Medical Physics, School of Allied Health Sciences, Faculty of Medicine, Osaka University, Suita, Osaka 565-0871, Japan. kohji.abe@shionogi.co.jp
pubmed:publicationType
Journal Article