Agmatine reverses pain induced by inflammation neuropathy and spinal cord injury

ECU Author/Contributor (non-ECU co-authors, if there are any, appear on document)

Kori L. Brewer (Creator)

Carolyn A. Fairbanks (Creator)

Brent M. Grocholski (Creator)

Lois J. Kehl (Creator)

Kelley F. Kitto (Creator)

H. Oanh Nguyen (Creator)

Soundararajan Regunathan (Creator)

Donald J. Reis (Creator)

Kristin L. Schreiber (Creator)

Don W. Shoeman (Creator)

Laura S. Stone (Creator)

George L. Wilcox (Creator)

Robert P. Yezierski (Creator)

Chen-Guang Yu (Creator)

Institution

East Carolina University (ECU )

Web Site: http://www.ecu.edu/lib/

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 (allodyniayhyperalgesia) 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. Originally published Proceedings of the National Academy of Sciences Vol. 97 No. 19 Sep 2000

Additional Information

Publication

Other

Proceedings of the National Academy of Sciences. 97:19(September 2000) p. 10584-10589.

Language: English

Date: 2011

Keywords

agmatine, nervous system plasticity, nerve injury, chronic pain

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