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"In summary, our present data demonstrated that, under the peripheral inflammatory pain condition, SDF1–CXCR4 signaling between non-neuronal SGCs and primary nociceptor neurons is dramatically enlarged through up-regulation of both substances in the DRG which acts as a mediator for the intraganglionar neuroinflammatory microenvironment and induces ERK-dependent up-regulation of Nav1.8 that contributes to the maintaining process of primary nociceptor neuronal hyperexcitability that is required for maintenance of persistent spontaneous pain and hypersensitivity."