Impairment of Fos protein formation in the rat infarct borderzone by MK-801, but not by NBQX

Thomas Christensen, M B Jørgensen, Nils Henrik Diemer

    14 Citations (Scopus)

    Abstract

    In the present immunocytochemical study, we investigated the mechanism of Fos protein induction and the regional distribution of the Fos protein in brains of spontaneously hypertensive rats subjected to 2 h of permanent middle cerebral artery occlusion (MCAO). Rats were administered either saline or a glutamate receptor antagonist; the non-competitive NMDA receptor antagonist MK-801 or the AMPA receptor antagonist NBQX which are known to be able to reduce infarct size in MCA occluded rats. The saline treated rats showed presence of Fos protein in nerve cell nuclei throughout the cortical and striatal infarct borderzone, but no staining in the infarct core or contralateral hemisphere. MK-801 almost totally abolished this expression of Fos protein whereas NBQX had no significant effect on Fos protein expression. It is suggested that the Fos protein induction is due to repeated spreading depressions mediated by NMDA receptors in the infarct borderzone, and that Fos protein due to its persistence in the tissue can be used as a histochemical marker of borderzone tissue at risk for eventually becoming recruited in the infarct.
    Original languageEnglish
    JournalActa Neurologica Scandinavica
    Volume87
    Issue number6
    Pages (from-to)510-515
    Number of pages6
    ISSN0001-6314
    Publication statusPublished - 1993

    Keywords

    • Animals
    • Cerebral Cortex
    • Cerebral Infarction
    • Corpus Striatum
    • Cortical Spreading Depression
    • Dizocilpine Maleate
    • Energy Metabolism
    • Gene Expression Regulation
    • Male
    • Neurons
    • Proto-Oncogene Proteins c-fos
    • Quinoxalines
    • Rats
    • Rats, Inbred SHR
    • Receptors, N-Methyl-D-Aspartate

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