Abstract
Following injury, NMDAR activation in spinal cord dorsal horn (SCDH) neurons facilitates the generation of pain in response to low threshold inputs (allodynia). The NMDAR signals the phosphorylation of extracellular signal-regulated kinase (ERK1/2), a key player in injury-induced pain in different cell types. Glia and pro-inflammatory cytokines are implicated in the maintenance of inflammatory pain and the modulation of neuronal activity. However, the role of the NMDAR and neuronal-glial-cytokine interactions that initiate and maintain inflammatory pain is not well defined.
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