Regional cerebral protein synthesis after transient ischemia in the rat: effect of the AMPA antagonist NBQX.

Article date: 1992/6/8

PubMed ID: 1383888

Journal name: Neuroscience letters (ISSN: 0304-3940)


Normothermic rats with 12 min, complete cerebral ischemia were treated with the AMPA antagonist 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo (F) quinoxalinedione (NBQX) [10], which prevents CA1 pyramidal neuron loss. Twenty hours after ischemia, cerebral protein synthesis rate (CPSR) was measured autoradiographically using [35S]methionine. Ischemia caused a 38% decrease of CPSR in CA1, and postischemic treatment with NBQX caused a 66% decrease in this region. Also treatment with NBQX alone resulted in a decrease (22% in CA1) of the CPSR. Since some evidence exists that the neuroprotective effect of NBQX is related to blockade of the fast AMPA-mediated transmission, the further decrease of the postischemic CPSR in CA1 could be a mere side effect.

Author List: Frank L, Bruhn T, Diemer N H

Publication Types: Journal Article; Research Support, Non-U.S. Gov't

Substances mentioned in the article: Nerve Tissue Proteins; Quinoxalines; Sulfur Radioisotopes; 2,3-dioxo-6-nitro-7-sulfamoylbenzo(f)quinoxaline; Ibotenic Acid; alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Methionine;

Mesh terms: Animals; Autoradiography; Brain/drug effects; Ibotenic Acid/analogs & derivatives; Ischemic Attack, Transient/metabolism; Male; Methionine/metabolism; Nerve Tissue Proteins/biosynthesis; Neurons/drug effects; Organ Specificity; Quinoxalines/pharmacology; Rats; Rats, Wistar; Sulfur Radioisotopes; alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid;

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