Endogenous interleukin-1β in neuropathic rats enhances glutamate release from the primary afferents in the spinal dorsal horn through coupling with presynaptic N-methyl-D-aspartic acid receptors

Abstract

Background: Excessive activation of glutamate receptors is crucial to the genesis of neuropathic pain. Results: Endogenous IL-1β in neuropathic rats enhances glutamate release by increasing presynapticNMDAreceptor activities via sphingomyelinase signaling. Conclusion: Coupling between IL-1β receptors and presynaptic NMDA receptors contributes to the genesis of neuropathic pain. Significance: Interruption of such coupling could be an effective approach for the treatment of neuropathic pain. © 2013 by The American Society for Biochemistry and Molecular Biology, Inc.