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    J Neuroimmunol. 2007 Mar;184(1-2):172-9. Epub 2007 Feb 2.

    Stimulation of prostaglandin E2-EP3 receptors exacerbates stroke and excitotoxic injury.

    Ahmad M, Ahmad AS, Zhuang H, Maruyama T, Narumiya S, Doré S.

    Source

    Department of Anesthesiology/Critical Care Medicine, Johns Hopkins University, School of Medicine, Baltimore, Maryland, USA.

    Abstract

    The effect of PGE(2) EP3 receptors on injury size was investigated following cerebral ischemia and induced excitotoxicity in mice. Treatment with the selective EP3 agonist ONO-AE-248 significantly and dose-dependently increased infarct size in the middle cerebral artery occlusion model. In a separate experiment, pretreatment with ONO-AE-248 exacerbated the lesion caused by N-methyl-d-aspartic acid-induced acute excitotoxicity. Conversely, genetic deletion of EP3 provided protection against N-methyl-d-aspartic acid-induced toxicity. The results suggest that PGE(2), by stimulating EP3 receptors, can contribute to the toxicity associated with cyclooxygenase and that antagonizing this receptor could be used therapeutically to protect against stroke- and excitotoxicity-induced brain damage.

    PMID:
    17275922
    [PubMed - indexed for MEDLINE]
    PMCID:
    PMC1914218
    Free PMC Article

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