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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Prostaglandin E2 Receptor EP4 Contributes to Inflammatory Pain Hypersensitivity.

Prostaglandin E(2) (PGE(2)) is both an inflammatory mediator released at the site of tissue inflammation and a neuromodulator that alters neuronal excitability and synaptic processing. The effects of PGE(2) are mediated by four G-protein-coupled EP receptors (EP1-EP4). Here we show that the EP4 receptor subtype is expressed by a subset of primary sensory dorsal root ganglion (DRG) neurons, and that its levels, but not that of the other EP1-3 subtypes, increase in the DRG after complete Freund' adjuvant-induced peripheral inflammation. Administration of both an EP4 antagonist [AH23848, (4Z)-7-[(rel-1S,2S,5R)-5-((1,1'-biphenyl-4-yl)methoxy)-2-(4-morpholinyl)-3-oxocyclopentyl]-4-heptenoic acid] and EP4 knockdown with intrathecally delivered short hairpin RNA attenuates inflammation-induced thermal and mechanical behavioral hypersensitivity, without changing basal pain sensitivity. AH23848 also reduces the PGE(2)-mediated sensitization of capsaicin-evoked currents in DRG neurons in vitro. These data suggest that EP4 is a potential target for the pharmacological treatment of inflammatory pain.[1]


  1. Prostaglandin E2 Receptor EP4 Contributes to Inflammatory Pain Hypersensitivity. Lin, C.R., Amaya, F., Barrett, L., Wang, H., Takada, J., Samad, T.A., Woolf, C.J. J. Pharmacol. Exp. Ther. (2006) [Pubmed]
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