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.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Aging / pathology
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Alprostadil / analogs & derivatives*
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Alprostadil / pharmacology
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Animals
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Brain Ischemia / pathology
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Brain Ischemia / physiopathology*
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Cell Death / physiology
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Cerebral Infarction / pathology
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Chronic Disease
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Excitatory Amino Acid Agonists / pharmacology
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Hippocampus / pathology
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Mice
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Mice, Inbred C57BL
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Mice, Knockout
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N-Methylaspartate / pharmacology
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Neurons / pathology
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Rats
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Rats, Sprague-Dawley
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Receptors, Prostaglandin E / agonists
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Receptors, Prostaglandin E / genetics
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Receptors, Prostaglandin E / physiology*
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Receptors, Prostaglandin E, EP2 Subtype
Substances
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Excitatory Amino Acid Agonists
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Ptger2 protein, mouse
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Receptors, Prostaglandin E
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Receptors, Prostaglandin E, EP2 Subtype
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N-Methylaspartate
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Alprostadil
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butaprost