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Persistent inflammatory nociception increases levels of dynorphin 1-17 in the spinal cord, but not in supraspinal nuclei involved in pain modulation. J Pain 2002 Aug;3(4):330-6

Date

11/19/2003

Pubmed ID

14622757

DOI

10.1054/jpai.2002.125185

Scopus ID

2-s2.0-0036342448 (requires institutional sign-in at Scopus site)   18 Citations

Abstract

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.

Author List

Parra MC, Nguyen TN, Hurley RW, Hammond DL

Author

Robert W. Hurley MD, PhD Adjunct Professor of Anesthesiology and CTSI in the Anesthesiology department at Medical College of Wisconsin