DeltaFosB, a stable splice variant of FosB, has been proposed to mediate persistent brain adaptation in response to several chronic perturbations, but it has not yet been considered in the context of sustained pain. Inflammatory pain induces neuronal plasticity that can result in persistent alteration of nociceptive pathways. This neuronal plasticity can partly result from changes in gene expression controlled by transcription factors. In the present study, we analyse the capacity of carrageenan-mediated inflammation to induce DeltaFosB in the spinal cord. We found that hind-paw inflammation increases FosB-like immunoreactivity in the superficial layers of rat lumbar spinal cord for at least 7 days. This induction parallels mechanical hyperalgesia and is maximal in the dorsal horn of segment L4 of the spinal cord which corresponds to the primary nociceptive afferent regions from the hind paw. We identified this FosB-like signal as DeltaFosB by comparing data obtained with antibodies raised against either an epitope present in both FosB and DeltaFosB, or the FosB C-terminal region that is deleted in DeltaFosB. The week-lasting changes in DeltaFosB highlight the interest in this protein as a molecular marker of sustained pain, and suggest a role of this transcription factor in pain-related plasticity within the spinal cord.