Prostaglandins, glutamate and nitric oxide synthase mediate nitroglycerin-induced hyperalgesia in the formalin test

Cristina Tassorelli, Rosaria Greco, Dechun Wang, Giorgio Sandrini, Giuseppe Nappi

Research output: Contribution to journalArticlepeer-review

Abstract

Increasing evidence supports a possible role for nitric oxide (NO) in the transmission of pain signals and in the development of central mechanisms of hyperalgesia. Previously, we have shown that nitroglycerin, an NO donor, is able to induce a long-lasting hyperalgesic state in rats. Nitroglycerin-induced hyperalgesia can be detected as an increase in the nociceptive behavior evoked by the formalin test. In the present study we investigated the possible mediators in the nitroglycerin-induced hyperalgesic state. Male Sprague-Dawley rats were injected with nitroglycerin and pretreated with indomethacin, 5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclo-hepten-5,10-imine hydrogen maleate (MK-801) or Nω-nitro-l-arginine methyl ester (l-NAME). The results obtained showed that inhibition of prostaglandins or NO synthesis prevents nitroglycerin-induced hyperalgesia in Phase II of the formalin test. A similar inhibitory effect was also observed following pretreatment with the glutamate antagonist MK801. The present findings point to the role of prostaglandins, NO synthesis and glutamate activity in the induction of nitroglycerin-induced hyperalgesia.

Original languageEnglish
Pages (from-to)103-107
Number of pages5
JournalEuropean Journal of Pharmacology
Volume534
Issue number1-3
DOIs
Publication statusPublished - Mar 18 2006

Keywords

  • Formalin test
  • Hyperalgesia
  • Indomethacin
  • L-NAME
  • MK-801
  • Nitric oxide

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience
  • Pharmacology

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