Effects of agmatine, interleukin-10, and cyclosporin on spontaneous pain behavior after excitotoxic spinal cord injury in rats

Chen Guang Yu, Carolyn A. Fairbanks, George L. Wilcox, Robert P. Yezierski

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59 Scopus citations


Intraspinal injection of the AMPA/metabotropic receptor agonist quisqualic acid (QUIS) results in a pathophysiology that leads to excessive grooming behavior, which has been proposed as a model of spontaneous at-level pain after spinal cord injury (SCI). To further characterize the onset and progression of this behavior we evaluated the effects of 3 drugs, agmatine (Agm), interleukin-10 (IL-10), and cyclosporin A (CsA), on different characteristics of this behavior. In these experiments rats were given saline, Agm, CsA10, or CsA20 once daily for 14 days (or a single injection of IL-10) starting either 30 minutes post-QUIS (group 1) or 10 to 18 days post-QUIS when excessive grooming behavior had been established (group 2). In the first group of animals agmatine, IL-10, CsA10, or CsA20 reduced the longitudinal extent of neuronal loss in the spinal cord compared to QUIS-injected animals treated with saline. The behavioral consequences of this effect included the delayed onset of excessive grooming behavior, reduction in the area of skin targeted for excessive grooming, and reduced grooming severity. Animals treated at the time of excessive grooming onset showed significantly reduced grooming area, grooming severity, and neuronal loss in the spinal cord compared to QUIS animals treated with saline. In conclusion, systemic administration of Agm, IL-10, or CsA significantly delayed the onset and reduced the severity of a spontaneous pain-like behavior. These effects are believed to be due, in part, to the neuroprotective properties of these drugs against QUIS-induced excitotoxicity. The effective treatment of excessive grooming behavior suggests that Agm, IL-10, and CsA modulate ongoing cellular events responsible for the progression of this behavior.

Original languageEnglish
Pages (from-to)129-140
Number of pages12
JournalJournal of Pain
Issue number3
StatePublished - Apr 2003

Bibliographical note

Funding Information:
Received July 15, 2002; Revised September 30, 2002; Accepted October 11, 2002 From the *Departments of Orthodontics and‖Neuroscience and the ¶McKnight Brain Institute, University of Florida, Gainesville, FL, and the Departments of †Pharmaceutics, ‡Pharmacology, and §Neuroscience, University of Minnesota, Minneapolis, MN. Supported by grants from the Hollfelder Foundation, NS40096 (R.P.Y.), DA11236 (G.L.W.), University of Minnesota Academic Health Center, and NCCAM training grant P50AT00009-02 (C.A.F.). Address reprint requests to Robert P. Yezierski, PhD, PO Box 100444, 1600 SW Archer Road, Gainesville, FL 32610. E-mail: [email protected] © 2003 by the American Pain Society 1526-5900/2003 $30.00 + 0 doi:10.1054/jpai.2003.11


  • Central pain
  • Immune function
  • Inflammation
  • NMDA receptors
  • Neuroprotection
  • Nitric oxide
  • Quisqualic acid
  • Spinal injury

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology
  • Anesthesiology and Pain Medicine


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