Discrepancy between cell injury and benzodiazepine receptor binding after transient middle cerebral artery occlusion in rats

Koji Abe, Yuto Kashiwagi, Miwa Tokumura, Rie Hosoi, Jun Hatazawa, Osamu Inoue

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)234-239
Number of pages6
JournalSynapse
Volume53
Issue number4
DOIs
Publication statusPublished - Sep 15 2004
Externally publishedYes

Fingerprint

Middle Cerebral Artery Infarction
GABA-A Receptors
Reperfusion
Middle Cerebral Artery
Ischemia
Wounds and Injuries
Cerebral Cortex
Flumazenil
Dopamine D1 Receptors
Transient Ischemic Attack
Muscarinic Receptors
Reperfusion Injury
Ligands
SCH 23390

Keywords

  • Autoradiography
  • Benzodiazepine receptor
  • Dopamine D receptor
  • Infarction
  • Middle cerebral artery occlusion
  • Muscarinic acetylcholine receptor
  • Rats

ASJC Scopus subject areas

  • Neuroscience(all)
  • Physiology
  • Pharmacology

Cite this

Discrepancy between cell injury and benzodiazepine receptor binding after transient middle cerebral artery occlusion in rats. / Abe, Koji; Kashiwagi, Yuto; Tokumura, Miwa; Hosoi, Rie; Hatazawa, Jun; Inoue, Osamu.

In: Synapse, Vol. 53, No. 4, 15.09.2004, p. 234-239.

Research output: Contribution to journalArticle

Abe, Koji ; Kashiwagi, Yuto ; Tokumura, Miwa ; Hosoi, Rie ; Hatazawa, Jun ; Inoue, Osamu. / Discrepancy between cell injury and benzodiazepine receptor binding after transient middle cerebral artery occlusion in rats. In: Synapse. 2004 ; Vol. 53, No. 4. pp. 234-239.
@article{7194a131c8e84e6dbb011d7c878ecc20,
title = "Discrepancy between cell injury and benzodiazepine receptor binding after transient middle cerebral artery occlusion in rats",
abstract = "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.",
keywords = "Autoradiography, Benzodiazepine receptor, Dopamine D receptor, Infarction, Middle cerebral artery occlusion, Muscarinic acetylcholine receptor, Rats",
author = "Koji Abe and Yuto Kashiwagi and Miwa Tokumura and Rie Hosoi and Jun Hatazawa and Osamu Inoue",
year = "2004",
month = "9",
day = "15",
doi = "10.1002/syn.20057",
language = "English",
volume = "53",
pages = "234--239",
journal = "Synapse",
issn = "0887-4476",
publisher = "Wiley-Liss Inc.",
number = "4",

}

TY - JOUR

T1 - Discrepancy between cell injury and benzodiazepine receptor binding after transient middle cerebral artery occlusion in rats

AU - Abe, Koji

AU - Kashiwagi, Yuto

AU - Tokumura, Miwa

AU - Hosoi, Rie

AU - Hatazawa, Jun

AU - Inoue, Osamu

PY - 2004/9/15

Y1 - 2004/9/15

N2 - 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.

AB - 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.

KW - Autoradiography

KW - Benzodiazepine receptor

KW - Dopamine D receptor

KW - Infarction

KW - Middle cerebral artery occlusion

KW - Muscarinic acetylcholine receptor

KW - Rats

UR - http://www.scopus.com/inward/record.url?scp=3843059189&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=3843059189&partnerID=8YFLogxK

U2 - 10.1002/syn.20057

DO - 10.1002/syn.20057

M3 - Article

C2 - 15266555

AN - SCOPUS:3843059189

VL - 53

SP - 234

EP - 239

JO - Synapse

JF - Synapse

SN - 0887-4476

IS - 4

ER -