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Publication : Ketamine does not produce relief of neuropathic pain in mice lacking the β-common receptor (CD131).

First Author  Swartjes M Year  2013
Journal  PLoS One Volume  8
Issue  8 Pages  e71326
PubMed ID  23936499 Mgi Jnum  J:205770
Mgi Id  MGI:5546437 Doi  10.1371/journal.pone.0071326
Citation  Swartjes M, et al. (2013) Ketamine does not produce relief of neuropathic pain in mice lacking the beta-common receptor (CD131). PLoS One 8(8):e71326
abstractText  Neuropathic pain (NP) is a debilitating condition associated with traumatic, metabolic, autoimmune and neurological etiologies. Although the triggers for NP are diverse, there are common underlying pathways, including activation of immune cells in the spinal cord and up-regulation of the N-methyl-D-aspartate receptor (NMDAR). Ketamine, a well-known NDMAR antagonist, reduces neuropathic pain in a sustained manner. Recent study has shown that the novel 11-amino acid peptide erythropoietin derivative ARA290 produces a similar, long-lasting relief of NP. Here, we show that both drugs also have similar effects on the expression of mRNA of the NMDAR, as well as that of microglia, astrocytes and chemokine (C-C motif) ligand 2, all-important contributors to the development of NP. Although the effects of ketamine and ARA 290 on NP and its molecular mediators suggest a common mechanism of action, ARA 290 has no affinity for the NMDAR and acts specifically via the innate repair receptor (IRR) involved in tissue protection. We speculated therefore, that the IRR might be critically involved in the action of ketamine on neuropathic pain. To evaluate this, we studied the effects of ketamine and ARA 290 on acute pain, side effects, and allodynia following a spared nerve injury model in mice lacking the beta-common receptor (betacR), a structural component of the IRR. Ketamine (50 mg/kg) and ARA 290 (30 microg/kg) produced divergent effects on acute pain: ketamine produced profound antinociception accompanied with psychomotor side effects, but ARA290 did not, in both normal and knock out mice. In contrast, while both drugs were antiallodynic in WT mice, they had no effect on NP in mice lacking the betacR. Together, these results show that an intact IRR is required for the effective treatment of NP with either ketamine or ARA 290, but is not involved in ketamine's analgesic and side effects.
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