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We investigated the temporal profile of heat shock protein 70 induction in the rat hippocampus using immunohistochemistry to clarify the mechanism of ischemic tolerance following preconditioning with sublethal ischemia. Although a 6-min period of forebrain ischemia produced severe neuronal damage to the hippocampal CA1 subfield, preconditioning with 3 min(More)
We examined whether preconditioning with sublethal ischemia protects against neuronal damage following subsequent lethal ischemic insults. Forebrain ischemia for 3 min in Wistar rats increased heat shock protein-70 immunoreactivity in the hippocampal CA1 subfield but produced no neuronal damage. Preconditioning with 3 min of ischemia followed by 3 days of(More)
To clarify the role of heat shock protein-70 (HSP70) in ischaemic tolerance following pretreatment with sublethal cerebral ischaemia, we examined whether the induction of tolerance in the gerbil hippocampus is inhibited by quercetin, an inhibitor of HSP70 expression, or anti-HSP70 antibody. A 3 min period of forebrain ischaemia was induced following(More)
To clarify the role of serotonin in cerebral ischemia, we examined the effects of selective serotonin reuptake inhibitors, citalopram and clomipramine, on ischemic neuronal damage in the gerbil. Pretreatment with citalopram (40 mg/kg i.p.) and clomipramine (20 mg/kg i.p.) protected against neuronal destruction of hippocampal CA1 pyramidal cells following 5(More)
We investigated the changes of copper/zinc superoxide dismutase (CuZn-SOD) and manganese superoxide dismutase (Mn-SOD) in the rat hippocampus after 10 min of cerebral ischemia induced by 4-vessel occlusion. The rats were allowed to survive for 4 h, 1 day, 3 days, and 7 days after ischemia. The distribution of SODs were determined by immunohistochemical(More)
Using immunohistochemistry, we visualized the localization of ubiquitin in the gerbil hippocampus following 3 min of ischemia with or without pretreatment with 2 min of sublethal ischemia and 3 days of reperfusion. Ubiquitin immunoreactivity in the hippocampus disappeared 4 h after 3 min of ischemia both with and without pretreatment. The immunoreactivity(More)
We examined the effects of treatment with basic fibroblast growth factor (b-FGF) on hippocampal CA1 neuronal damage following 3 min of forebrain ischemia in the gerbil. Continuous infusion of b-FGF (24 or 240 ng/day over 4 days) using an implanted osmotic minipump into the lateral ventricle prevented CA1 neuronal damage in a dose-dependent manner.
The effects of prostaglandin (PG) E2 on glutamate-induced cytotoxicity were examined using primary cultures of rat cortical neurons. The cell viability was significantly reduced when cultures were briefly exposed to either glutamate or N-methyl-D-aspartate (NMDA) then incubated with normal medium for 1 h. Similar cytotoxicity was observed with the brief(More)
The project also received supplementary support and funding from the American Iron and Steel Institute. Project updates are available at www.ce.jhu.edu/cfsnees. Any opinions, findings, and conclusions or recommendations expressed in this publication are those of the author(s) and do not necessarily reflect the views of the National Science Foundation, nor(More)
Preconditioning of the gerbil brain with a 2-min period of sublethal ischemia followed by 4 days of reperfusion protects against neuronal damage following a subsequent 3-min period of ischemia, which normally destroys pyramidal neurons in the CA1 region of the hippocampus. To clarify the role of protein synthesis in this ischemic tolerance phenomenon, we(More)