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Research ArticleArticle

Chelation of Zinc in the Extracellular Area of the Spinal Cord, Using Ethylenediaminetetraacetic Acid Disodium-Calcium Salt or Dipicolinic Acid, Inhibits the Antinociceptive Effect of Capsaicin in Adult Mice

Alice A. Larson and Kelley F. Kitto
Journal of Pharmacology and Experimental Therapeutics February 1999, 288 (2) 759-765;
Alice A. Larson
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Kelley F. Kitto
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Abstract

Capsaicin depolarizes primary afferent C-fibers releasing substance P (SP) whose N-terminal metabolites appear to play a role in the development of antinociception. Because some effects of SP(1–7) are similar to those of zinc, we tested the hypothesis that zinc in the extracellular area plays a role in capsaicin-induced antinociception, as measured using the abdominal stretch (writhing) assay. Decreases in zinc were achieved by intrathecal (i.t.) injection of membrane-impermeable compounds: ethylenediaminetetraacetic acid disodium-calcium salt (Ca++ EDTA), a calcium-saturated chelator of divalent cations, or dipicolinic acid, a zinc chelator. Ten nanomoles of Ca++ EDTA had no effect on writhing at either 90 min or 24 h after injection, yet pretreatment with Ca++ EDTA prevented the development of antinociception 24 h after i.t. injection of either 2.8 nmol of capsaicin or 10 nmol of SP(1–7). One nanomole of dipicolinic acid injected i.t. also blocked capsaicin- and SP(1–7)-induced antinociception. When injected 24 h after SP(1–7), Ca++ EDTA failed to reverse antinociception. Acute antinociception produced 30 min after injection of SP(1–7) was also blocked when Ca++ EDTA was injected 24 h, but not 60 min, before SP(1–7). Thus, the optimal time of Ca++ EDTA-induced hyperalgesia (90 min), described previously, did not correspond to that of its inhibitory effect on antinociception (24 h). In contrast, we found that the previously described antinociception after an i.t. injection of zinc (90 min) is greatly attenuated by 24 h. Thus, zinc appears to be necessary, but may not be sufficient, for the long-term antinociceptive effect of capsaicin, acting downstream from the action of substance P N-terminal metabolites.

Footnotes

  • Send reprint requests to: Dr. Alice A. Larson, Department of Veterinary Pathobiology, University of Minnesota, 295 Animal Science/Veterinary Medicine Building, 1988 Fitch Ave., St. Paul, MN 55108. E-mail: larso011{at}tc.umn.edu

  • ↵1 This work was supported by United States Public Health Service Grant DA04090 (A.A.L.).

  • Abbreviations:
    Ca++ EDTA
    ethylenediaminetetraacetic acid disodium-calcium salt
    CNS
    central nervous system
    NMDA
    N-methyl-d-aspartate
    SP
    substance P
    • Received February 13, 1998.
    • Accepted September 5, 1998.
  • The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics: 288 (2)
Journal of Pharmacology and Experimental Therapeutics
Vol. 288, Issue 2
1 Feb 1999
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Research ArticleArticle

Chelation of Zinc in the Extracellular Area of the Spinal Cord, Using Ethylenediaminetetraacetic Acid Disodium-Calcium Salt or Dipicolinic Acid, Inhibits the Antinociceptive Effect of Capsaicin in Adult Mice

Alice A. Larson and Kelley F. Kitto
Journal of Pharmacology and Experimental Therapeutics February 1, 1999, 288 (2) 759-765;

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Research ArticleArticle

Chelation of Zinc in the Extracellular Area of the Spinal Cord, Using Ethylenediaminetetraacetic Acid Disodium-Calcium Salt or Dipicolinic Acid, Inhibits the Antinociceptive Effect of Capsaicin in Adult Mice

Alice A. Larson and Kelley F. Kitto
Journal of Pharmacology and Experimental Therapeutics February 1, 1999, 288 (2) 759-765;
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