Neuroprotection by the PGE2 EP2 receptor in permanent focal cerebral ischemia

Ann Neurol. 2005 May;57(5):758-61. doi: 10.1002/ana.20461.

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

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Aging / pathology
  • Alprostadil / analogs & derivatives*
  • Alprostadil / pharmacology
  • Animals
  • Brain Ischemia / pathology
  • Brain Ischemia / physiopathology*
  • Cell Death / physiology
  • Cerebral Infarction / pathology
  • Chronic Disease
  • Excitatory Amino Acid Agonists / pharmacology
  • Hippocampus / pathology
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • N-Methylaspartate / pharmacology
  • Neurons / pathology
  • Rats
  • Rats, Sprague-Dawley
  • Receptors, Prostaglandin E / agonists
  • Receptors, Prostaglandin E / genetics
  • Receptors, Prostaglandin E / physiology*
  • Receptors, Prostaglandin E, EP2 Subtype

Substances

  • Excitatory Amino Acid Agonists
  • Ptger2 protein, mouse
  • Receptors, Prostaglandin E
  • Receptors, Prostaglandin E, EP2 Subtype
  • N-Methylaspartate
  • Alprostadil
  • butaprost