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Neuroprotection by the PGE2 EP2 receptor in permanent focal cerebral ischemia

Authors

  • Dong Liu PhD,

    1. Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center, Baltimore, MD
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  • Liejun Wu BS,

    1. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD
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  • Richard Breyer PhD,

    1. Department of Medicine, division of Nephrology, Vanderbilt University School of Medicine, Nashville, TN
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  • Mark P. Mattson PhD,

    1. Laboratory of Neurosciences, National Institute on Aging Gerontology Research Center, Baltimore, MD
    2. Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD
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  • Katrin Andreasson MD

    Corresponding author
    1. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD
    2. Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD
    • Department of Neurology, Johns Hopkins University School of Medicine, 600 N. Wolfe Street, Meyer 5-119B, Baltimore, MD 21205
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Abstract

Recent studies suggest a neuroprotective function of the PGE2 EP2 receptor in excitotoxic neuronal injury. The function of the EP2 receptor was examined at time points after excitotoxicity in an organotypic hippocampal model of N-methyl-D-aspartate (NMDA) challenge and in a permanent model of focal forebrain ischemia. Activation of EP2 led to significant neuroprotection in hippocampal slices up to 3 hours after a toxic NMDA stimulus. Genetic deletion of EP2 resulted in a marked increase in stroke volume in the permanent middle cerebral artery occlusion model. These findings support further investigation into therapeutic strategies targeting the EP2 receptor in stroke. Ann Neurol 2005;57:758–761

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