Microglial inhibition of neuroprotection by antagonists of the EP1 prostaglandin E2 receptor

J Neuroinflammation. 2009 Feb 17:6:5. doi: 10.1186/1742-2094-6-5.

Abstract

Background: The EP1 receptor for the prostanoid PGE2 is a G-protein coupled receptor that has been shown to contribute to excitotoxic neuronal death. In this study we examined the influence of non-neuronal cells on neuroprotective properties of EP1 receptor antagonists (Ono 8711 and SC 51089).

Methods: Primary neuronal cultures systems with or without non-neuronal cells were used to examine how the neuroprotective properties of EP1 antagonists were influenced by non-neuronal cells. The influence of astrocytes or microglia were individually tested in excitotoxicity assays using a co-culture system with these cells grown on permeable transwell inserts above the neuronal-enriched cultures. The influence of microglia on PGE2 synthesis and EP1 receptor expression was examined.

Results: EP1 antagonists were neuroprotective in neuronal-enriched cultures (> 90% neurons) but not in mixed cultures (30% neurons plus other non-neuronal cells). Co-cultures of microglia on permeable transwell inserts above neuronal-enriched cultures blocked neuroprotection by EP1 antagonists. Incubation of microglia with neuronal-enriched cultures for 48 hours prior to NMDA challenge was sufficient to block neuroprotection by EP1 antagonists. The loss of neuroprotection by EP1 antagonists was accompanied by a decrease of neuronal EP1 expression in the nucleus in cultures with microglia present.

Conclusion: These findings demonstrate microglial modulation of neuronal excitotoxicity through interaction with the EP1 receptor and may have important implications in vivo where microglia are associated with neuronal injury.

Publication types

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

MeSH terms

  • Animals
  • Astrocytes / physiology
  • Bridged Bicyclo Compounds / pharmacology
  • Caproates / pharmacology
  • Cell Death / drug effects
  • Cell Death / physiology
  • Cells, Cultured
  • Coculture Techniques
  • Cyclooxygenase 2 Inhibitors / pharmacology
  • Dinoprostone / metabolism
  • Dose-Response Relationship, Drug
  • Excitatory Amino Acid Agonists / toxicity
  • Hydrazines / pharmacology
  • Mice
  • Microglia / physiology*
  • Microscopy, Confocal
  • N-Methylaspartate / toxicity
  • Neurons / drug effects*
  • Neurons / physiology
  • Neuroprotective Agents / pharmacology*
  • Oxazepines / pharmacology
  • Receptors, Prostaglandin E / antagonists & inhibitors*
  • Receptors, Prostaglandin E / metabolism
  • Receptors, Prostaglandin E, EP1 Subtype

Substances

  • Bridged Bicyclo Compounds
  • Caproates
  • Cyclooxygenase 2 Inhibitors
  • Excitatory Amino Acid Agonists
  • Hydrazines
  • Neuroprotective Agents
  • ONO 8711
  • Oxazepines
  • Ptger1 protein, mouse
  • Receptors, Prostaglandin E
  • Receptors, Prostaglandin E, EP1 Subtype
  • SC 51089
  • N-Methylaspartate
  • Dinoprostone