Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 99, Issue 4, Pages 2362-2367Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.261713299
Keywords
ischemia; neuronal death; glutamate receptors; alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid receptors; ischemic tolerance
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Funding
- NINDS NIH HHS [NS31282, NS20752, R01 NS020752, NS07512] Funding Source: Medline
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Animals subjected to sublethal transient global ischemia (ischemic preconditioning) exhibit neuroprotection against subsequent global ischemia-induced neuronal death in the hippocampal CA1 (ischemic tolerance). The molecular mechanisms underlying ischemic tolerance are unclear. Here we report that ischernic preconditioning induced a small,. transient down-regulation of GluR2 mRNA expression and greatly attenuated subsequent ischemia-induced GluR2 mRNA and protein down-regulation and neuronal death. Ischemic preconditioning and GluR2 antisense knockdown acted synergistically to increase cell death. Sublethal antisense knockdown did not protect against subsequent ischemic insults or antisense knockdown. These findings indicate that ischemic preconditioning acts at step(s) upstream from suppression of GluR2 gene expression to afford neuroprotection and implicate transcriptional regulation of GluR2 expression in the adaptive mechanisms associated with ischernic tolerance.
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