Persistent inflammatory nociception increases levels of dynorphin 1-17 in the spinal cord, but not in supraspinal nuclei involved in pain modulation.

It is well established that nerve injury or inflammatory injury results in a time-dependent increase in the expression of dynorphin in the spinal cord. However, little is known about the effects of persistent pain on the expression of this endogenous opioid peptide by supraspinal nuclei implicated in the modulation of pain sensitivity. This study used enzyme-linked immunosorbent assay to measure the levels of dynorphin(1-17) in the spinal cord as well as in brainstem nuclei 4 hours, 4 days, or 2 weeks after intraplantar injection of saline or complete Freund's adjuvant in the left hind paw. As previously reported, complete Freund adjuvant produced a time-dependent increase in dynorphin that was confined to the ipsilateral dorsal horn. In contrast, levels of dynorphin(1-17) in the nucleus raphe magnus, nucleus reticularis gigantocellularis pars alpha, parabrachial nuclei, microcellular tegmentum, pontine periaqueductal gray, and midbrain periaqueductal gray were not affected at any time after injection of complete Freund adjuvant. These data suggest that alterations in levels of dynorphin do not mediate the up-regulation of activity in bulbospinal pain inhibitory or pain facilitatory pathways that occurs during persistent pain.