title: Extended neuronal protection induced after sublethal ischemia adjacent to the area with delayed neuronal death.
abstract: In the present study, we investigated whether neurons adjacent to an ischemic lesion acquire tolerance against subsequent ischemia or not. We initially used unilateral hemispheric ischemia for 3 min in gerbils to produce an ischemic lesion confined to the unilateral CA1 sector, and the presence of tolerance was examined in the adjacent CA3 sector through transient global ischemia by occlusion of both common carotid arteries. Attenuation of neuronal damage was clearly observed in neurons in the CA3 sector adjacent to the ischemic lesion in the CA1 sector. The phenomenon lasted for up to two weeks after the initial hemispheric ischemia, but was no longer present two months later. Reactive astrocytes as identified by the presence of glial fibrillary acidic protein were visible in the CA3 hippocampus four days and two weeks after hemispheric ischemia, but they were scarce two months later. Expression of heat shock protein 72 in the CA3 neurons was observed four days after hemispheric ischemia, but the reaction returned to the control level two weeks later. In conclusion, the present study showed that tolerance in the neurons adjacent to an ischemic lesion could be sustained at least for two weeks, and raised the possibility that reactive astrocytes might contribute to the extended tolerance in neurons.
authors.affiliation: Division of Strokology, Department of Internal Medicine and Therapeutics, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Kitagawa
authors.forename: M
authors.initials: M
authors.lastname: Matsumoto
authors.forename: T
authors.initials: T
authors.lastname: Ohtsuki
authors.forename: K
authors.initials: K
authors.lastname: Kuwabara
authors.forename: T
authors.initials: T
authors.lastname: Mabuchi
authors.forename: Y
authors.initials: Y
authors.lastname: Yagita
authors.forename: M
authors.initials: M
authors.lastname: Hori
authors.forename: T
authors.initials: T
authors.lastname: Yanagihara
mesh_terms: D000818:Animals; D001253:Astrocytes / Q000473:pathology; D002545:Brain Ischemia / Q000473:pathology / Q000503:physiopathology*; D016923:Cell Death / Q000502:physiology; D005260:Female; D005849:Gerbillinae; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D050884:HSP72 Heat-Shock Proteins; D006360:Heat-Shock Proteins / Q000378:metabolism; D006624:Hippocampus / Q000378:metabolism / Q000473:pathology; D008297:Male; D009474:Neurons / Q000502:physiology*; D013997:Time Factors
chemical_list: D005904:Glial Fibrillary Acidic Protein; D050884:HSP72 Heat-Shock Proteins; D006360:Heat-Shock Proteins