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Spinal ephrin B / EphB signalling contributed to remifentanil‐induced hyperalgesia via NMDA receptor
Author(s) -
Xia W.S.,
Peng Y.N.,
Tang L.H.,
Jiang L.S.,
Yu L.N.,
Zhou X.L.,
Zhang F.J.,
Yan M.
Publication year - 2014
Publication title -
european journal of pain
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.305
H-Index - 109
eISSN - 1532-2149
pISSN - 1090-3801
DOI - 10.1002/j.1532-2149.2014.00478.x
Subject(s) - hyperalgesia , nmda receptor , ephrin , agonist , receptor , chemistry , erythropoietin producing hepatocellular (eph) receptor , allodynia , pharmacology , nociception , receptor antagonist , remifentanil , antagonist , medicine , biochemistry , receptor tyrosine kinase , propofol
Background One of the major unresolved issues in treating pain is the paradoxical hyperalgesia produced by opiates, and accumulating evidence implicate that Eph B s receptors and ephrin B s ligands are involved in mediation of spinal nociceptive information and central sensitization, but the manner in which ephrin B / EphB signalling acts on spinal nociceptive information networks to produce hyperalgesia remains enigmatic. The objective of this research was to investigate the role of ephrin B / EphB signalling in remifentanil‐induced hyperalgesia ( RIH ) and its downstream effector. Methods We characterized the remifentanil‐induced pain behaviours by evaluating thermal hyperalgesia and mechanical allodynia in a rat hind paw incisional model. Protein expression of EphB 1 receptor and ephrin B 1 ligand in spinal dorsal horn cord was determined by Western blotting, and F os was determined by immunohistochemistry assay, respectively. To figure out the manner in which ephrin B / EphB signalling acts with N ‐methyl‐ d ‐aspartic acid ( NMDA ) receptor, we used MK ‐801, an antagonist of NMDA receptor, trying to suppressed the hyperalgesia induced by ephrin B 1‐ Fc , an agonist of ephrin B / EphB . Results Continuing infusion of remifentanil produced a thermal hyperalgesia and mechanical allodynia, which was accompanied with increased protein expression of spinal‐level EphB 1 receptor, ephrin B 1 ligand and F os; what appeared above was suppressed by pretreatment with EphB 1‐ Fc , an antagonist of ephrin B / EphB or MK ‐801, and increased pain behaviours induced by intrathecal injection of ephrin B 1‐ Fc , an agonist of ephrin B / EphB , were suppressed by MK ‐801. Conclusions Our findings indicated that ephrin B / EphB signalling is involved in RIH . Ephrin B / EphB signalling might be the upstream of NMDA receptor.