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

Spinal prostaglandin E receptors of the EP2 subtype and the glycine receptor alpha3 subunit, which mediate central inflammatory hyperalgesia, do not contribute to pain after peripheral nerve injury or formalin injection.

Inflammation, peripheral nerve injury and chemical irritants can cause central sensitization in pain pathways. Prostaglandins produced in the CNS induce central sensitization during inflammation mainly by relieving nociceptive neurons from glycinergic inhibition. We have recently identified spinal prostaglandin E receptors of the EP2 subtype ( EP2 receptors) and the glycine receptor alpha3 subunit (GlyRalpha3) as signal transduction elements involved in the generation of central inflammatory hyperalgesia. It is however still unknown to what extent inhibition of glycine receptors by PGE(2) contributes to neuropathic or chemically induced pain. To address this question, we have analyzed mice deficient in the EP2 receptor ( EP2(-/-) mice) or in the GlyRalpha3 subunit (GlyRalpha3(-/-) mice) using the chronic constriction injury (CCI) model of neuropathic pain and the formalin test. We found that EP2(-/-) mice and GlyRalpha3(-/-) mice develop thermal and mechanical hyperalgesia in the CCI model indistinguishable from that seen in wild-type mice. In the formalin test, EP2(-/-) mice, but not GlyRalpha3(-/-) mice, exhibited reduced nocifensive behavior. The lack of a phenotype in GlyRalpha3(-/-) mice together with the absence of a facilitating effect of intrathecal PGE(2) on formalin-induced nociception in wild-type mice suggests that peripheral rather than spinal EP2 receptors are involved. These results indicate that inhibition of glycinergic neurotransmission by EP2 receptor activation does not contribute to pain following peripheral nerve injury or chemical irritation with formalin. Our results thus provide further evidence that inflammatory hyperalgesia and neuropathic pain involve different mechanisms of central sensitization.[1]


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