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Volume 17, Number 24, Issue of December 15, 1997 pp. 9536-9544

Sublethal Oxygen-Glucose Deprivation Alters Hippocampal Neuronal AMPA Receptor Expression and Vulnerability to Kainate-Induced Death

Received June 6, 1997; revised Sept. 3, 1997; accepted Oct. 7, 1997.

Howard S. Ying1, Jochen H. Weishaupt2, Margaret Grabb1, Lorella M. T. Canzoniero1, Stefano L. Sensi1, Christian T. Sheline1, Hannah Monyer2, and Dennis W. Choi1

1 Center for the Study of Nervous System Injury and Department of Neurology, Washington University School of Medicine, St. Louis, Missouri 63110, and 2 Center for Molecular Biology (ZMBH), University of Heidelberg, 69120 Heidelberg, Germany

Recent studies have suggested that rats subjected to transient global brain ischemia develop depressed expression of GluR-B in CA1 hippocampal neurons. The present study was performed to determine whether a similar change in AMPA receptor expression could be triggered in vitro by sublethal oxygen-glucose deprivation in rat hippocampal neuronal cultures. mRNA was extracted from individual hippocampal neurons via patch electrodes and amplified by RT-PCR 24-48 hr after sublethal oxygen-glucose deprivation. Compared with controls, insulted neurons expressed increased levels of GluR-D flop. As an indication that this change in receptor expression was functionally significant, insulted cultures exhibited increased AMPA- or kainate-induced 45Ca2+ accumulation sensitive to Joro spider toxin and increased vulnerability to kainate-induced death. These data support the hypothesis that exposure to ischemia may enhance subsequent hippocampal neuronal vulnerability to AMPA receptor-mediated excitotoxicity by modifying the relative expression of AMPA receptor subunits in a manner that promotes Ca2+ permeability.

Key words: glutamate receptor regulation; GluR-D; single cell RT-PCR; calcium accumulation; ischemia; neuronal vulnerability




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