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- Title
Activation of Akt/Protein Kinase B Contributes to Induction of Ischemic Tolerance in the CA1 Subfield of Gerbil Hippocampus.
- Authors
Yano, Shigetoshi; Morioka, Motohiro; Fukunaga, Kohji; Kawano, Takayuki; Hara, Tsuyoshi; Kai, Yutaka; Hamada, Jun-ichiro; Miyamoto, Eishichi; Ushio, Yukitaka
- Abstract
SummaryApoptosis plays an important role in delayed neuronal cell death after cerebral ischemia. Activation of Akt/protein kinase B has been recently reported to prevent apoptosis in several cell types. In this article the authors examine whether induction of ischemic tolerance resulting from a sublethal ischemic insult requires Akt activation. Sublethal ischemia gradually and persistently stimulated phosphorylation of Akt-Ser-473 in the hippocampal CA1 region after reperfusion. After lethal ischemia, phosphorylation of Akt-Ser-473 showed no obvious decrease in preconditioned gerbils but a marked decrease in nonconditioned gerbils. Changes in Akt-Ser-473 phosphorylation were correlated with changes in Akt activities, as measured by an in vitro kinase assay. Intracerebral ventricular infusion of wortmannin before preconditioning blocked both the increase in Akt-Ser-473 phosphorylation in a dose-dependent manner and the neuroprotective action of preconditioning. These results suggest that Akt activation is induced by a sublethal ischemic insult in gerbil hippocampus and contributes to neuroprotective ischemic tolerance in CA1 pyramidal neurons.Journal of Cerebral Blood Flow & Metabolism (2001) 21, 351-360; doi:10.1097/00004647-200104000-00004
- Publication
Journal of Cerebral Blood Flow & Metabolism, 2001, Vol 21, Issue 4, p351
- ISSN
0271-678X
- Publication type
Article
- DOI
10.1097/00004647-200104000-00004