title: Time course of nitric oxide synthase activity in neuronal, glial, and endothelial cells of rat striatum following focal cerebral ischemia.
abstract: 1. The time course of nitric oxide synthase (NOS) activity in neuronal, endothelial, and glial cells in the rat striatum after middle cerebral artery (MCA) occlusion and reperfusion was examined using a histochemical NADPH-diaphorase staining method. 2. In sham-operated rats, neuronal cells of the striatum exhibited strong NADPH-diaphorase activities. When rats were subjected to MCA occlusion for 1 hr, neuronal damage, including neurons with positive NADPH-diaphorase activities, appeared in the striatum at 3 hr after and extended to all areas of the striatum 3-4 days after reperfusion. 3. NADPH-diaphorase activities in the endothelial cells increased in the damaged part of striatum from 3 hr after, peaked at 1-2 days after MCA occlusion/reperfusion, then gradually decreased. 4. In parallel with the development of neuronal damage, some astrocytes and a high proportion of microglia/macrophages located in the perisite and in the center of the damaged striatum, respectively, exhibited a moderate to high level of NADPH-diaphorase activities. Most of these activities disappeared at 4 days after MCA occlusion. 5. These findings provided evidence that an inappropriate activation of NOS in endothelial cells and microglia/macrophages, in response to MCA occlusion/reperfusion, is closely associated with initiation and progression of ischemic neuronal injury in the striatum.
authors.affiliation: Department of Hospital Pharmacy, Nagasaki University School of Medicine, Japan.
authors.forename: M N
authors.initials: MN
authors.lastname: Nakashima
authors.forename: K
authors.initials: K
authors.lastname: Yamashita
authors.forename: Y
authors.initials: Y
authors.lastname: Kataoka
authors.forename: Y S
authors.initials: YS
authors.lastname: Yamashita
authors.forename: M
authors.initials: M
authors.lastname: Niwa
mesh_terms: D000818:Animals; D001253:Astrocytes / Q000473:pathology; D002536:Cerebral Arteries; D003342:Corpus Striatum / Q000098:blood supply* / Q000201:enzymology* / Q000473:pathology; D004730:Endothelium, Vascular / Q000201:enzymology* / Q000473:pathology; D005904:Glial Fibrillary Acidic Protein / Q000032:analysis; D007150:Immunohistochemistry; D002546:Ischemic Attack, Transient / Q000201:enzymology* / Q000473:pathology; D007700:Kinetics; D008297:Male; D009252:NADPH Dehydrogenase / Q000378:metabolism; D009457:Neuroglia / Q000201:enzymology* / Q000473:pathology; D009474:Neurons / Q000201:enzymology* / Q000473:pathology; D019001:Nitric Oxide Synthase / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D015424:Reperfusion; D013997:Time Factors
chemical_list: D005904:Glial Fibrillary Acidic Protein; D019001:Nitric Oxide Synthase; D009252:NADPH Dehydrogenase