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Buprenorphine inhibits bradykinin-induced release of calcitonin gene-related peptide from rat trigeminal neurons via both μ-opioid and nociceptin/orphanin peptide receptors

In this study we used the dual opioid and nociceptin/orphanin peptide (NOP) agonist buprenorphine to investigate the relative contributions of opioid and NOP systems in regulating bradykinin-stimulated calcitonin-gene related peptide (CGRP) release from primary cultures of neonatal rat trigeminal ne...

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Bibliographic Details
Published in:European journal of pharmacology 2009-05, Vol.609 (1), p.45-50
Main Authors: Capuano, Alessandro, De Corato, Alice, Tringali, Giuseppe, Currò, Diego, Dello Russo, Cinzia, Navarra, Pierluigi
Format: Article
Language:English
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Summary:In this study we used the dual opioid and nociceptin/orphanin peptide (NOP) agonist buprenorphine to investigate the relative contributions of opioid and NOP systems in regulating bradykinin-stimulated calcitonin-gene related peptide (CGRP) release from primary cultures of neonatal rat trigeminal neurons. We found that: bradykinin stimulates CGRP secretion either by a direct effect or after applying so-called “bradykinin -priming” protocol. In both cases, buprenorphine was able to inhibit bradykinin-stimulated CGRP secretion; however, inhibition was mediated by NOP receptors when buprenorphine was added to the incubation medium along with bradykinin, whereas it appeared to be mediated by μ-opioid receptors in bradykinin priming experiments. Bradykinin treatments also caused an increase in neuronal prostaglandin production; prostanoids appeared to be involved in the stimulatory effects of bradykinin as well as in buprenorphine inhibition, through apparently unrelated mechanisms.
ISSN:0014-2999
1879-0712
DOI:10.1016/j.ejphar.2009.03.013