Abstract
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 mu-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.
Lingua originale | Inglese |
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pagine (da-a) | 45-50 |
Numero di pagine | 6 |
Rivista | European Journal of Pharmacology |
Stato di pubblicazione | Pubblicato - 2009 |
Keywords
- Bradfykinin
- Buprenorphine
- CGRP
- NOP receptor
- Rat trigeminal neurons