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The Journal of Neuroscience, June 15, 1999, 19(12):5026-5033

Attenuation of Ischemia-Induced Cellular and Behavioral Deficits by X Chromosome-Linked Inhibitor of Apoptosis Protein Overexpression in the Rat Hippocampus

Daigen Xu1, 2, Yves Bureau4, Dan C. McIntyre4, Donald W. Nicholson5, Peter Liston2, 3, Yanxia Zhu1, 2, Wei Gin Fong3, Stephen J. Crocker1, Robert G. Korneluk2, 3, and George S. Robertson1, 6

1 Department of Cellular and Molecular Medicine, Faculty of Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5, Canada, 2 Apoptogen and 3 Genetics Research Laboratory, Children's Hospital of Eastern Ontario, Ottawa, Ontario K1H 8L1, Canada, 4 Department of Psychology, Carleton University, Ottawa, Ontario K1S 5B6, Canada, and 5 Apoptosis Research Program, Department of Biochemistry and Molecular Biology and 6 Department of Pharmacology, Merck Frosst Centre for Therapeutic Research, Kirkland, Quebec H9H 3L1, Canada

Transient forebrain ischemia produced by four-vessel occlusion (4-VO) triggers the delayed death of CA1 neurons in the hippocampus, resulting in behavioral deficits of spatial learning performance. We demonstrate that CA1 neuronal loss induced by 4-VO (12 min) is preceded by a selective and marked elevation of catalytically active caspase-3 in these neurons, indicative of apoptosis. Virally mediated overexpression of the anti-apoptotic gene X chromosome-linked inhibitor of apoptosis protein (XIAP) prevented both the production of catalytically active caspase-3 and degeneration of CA1 neurons after transient forebrain ischemia. CA1 neurons protected in this manner appeared to function normally, as assessed by immunohistochemical detection of the neuronal activity marker nerve growth factor inducible-A and by spatial learning performance in the Morris water maze. These findings indicate that caspase-3 activation is a key event in ischemic neuronal death and that blockade of this event by XIAP overexpression permits CA1 neurons to survive and operate properly after an ischemic insult.

Key words: XIAP; caspase-3; DNA fragmentation; water maze; apoptosis; NGFI-A

Copyright © 1999 Society for Neuroscience  0270-6474/99/19125026-08$05.00/0


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