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.
Original language | English (US) |
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Pages (from-to) | 758-761 |
Number of pages | 4 |
Journal | Annals of Neurology |
Volume | 57 |
Issue number | 5 |
DOIs | |
State | Published - May 2005 |
ASJC Scopus subject areas
- Neuroscience(all)