Agmatine reverses pain induced by inflammation, neuropathy, and spinal cord injury

Carolyn A. Fairbanks, Kristin L. Schreiber, Kori L. Brewer, Chen Guang Yu, Laura S. Stone, Kelley F. Kitto, H. Oanh Nguyen, Brent M. Grocholski, Don W. Shoeman, Lois J. Kehl, Soundararajan Regunathan, Donald J. Reis, Robert P. Yezierski, George L. Wilcox

Research output: Contribution to journalArticlepeer-review

194 Scopus citations

Abstract

Antagonists of glutamate receptors of the N-methyl-D-aspartate subclass (NMDAR) or inhibitors of nitric oxide synthase (NOS) prevent nervous system plasticity. Inflammatory and neuropathic pain rely on plasticity, presenting a clinical opportunity for the use of NMDAR antagonists and NOS inhibitors in chronic pain. Agmatine (AG), an endogenous neuromodulator present in brain and spinal cord, has both NMDAR antagonist and NOS inhibitor activities. We report here that AG, exogenously administered to rodents, decreased hyperalgesia accompanying inflammation, normalized the mechanical hypersensitivity (allodynia/hyperalgesia) produced by chemical or mechanical nerve injury, and reduced autotomy-like behavior and lesion size after excitotoxic spinal cord injury. AG produced these effects in the absence of antinociceptive effects in acute pain tests. Endogenous AG also was detected in rodent lumbosacral spinal cord in concentrations similar to those previously detected in brain. The evidence suggests a unique antiplasticity and neuroprotective role for AG in processes underlying persistent pain and neuronal injury.

Original languageEnglish (US)
Pages (from-to)10584-10589
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Volume97
Issue number19
DOIs
StatePublished - Sep 12 2000

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