Abstract:
:The effects of phospholipase A2, cyclooxygenase-1, cyclooxygenase-2, and 5-lipoxygenase inhibitors on acute opiate withdrawal induced by selective mu, kappa and delta receptor agonists was investigated in vitro. After a 4 min in vitro exposure to D-Ala2-N-methyl-Phe-Gly5-ol)enkephalin (DAMGO; a highly selective mu agonist) and trans(+/-)-3,4-dichloro-N-methyl-N-(2(1pyrrolidynyl)-cyclohexyl)-+ ++benzeneacetamid (U50-488H; a highly selective K agonist) a strong contraction of the guinea pig isolated ileum was observed after the addition of naloxone. This effect was also observed when rabbit isolated jejunum was pretreated with deltorphin (a highly selective delta agonist). Mepacrine (a phospholipase A2 inhibitor), tolmetin (a selective cyclooxygenase-1 inhibitor) and meloxicam (a selective cyclooxygenase-2 inhibitor) treatment before or after DAMGO or U50-488H were able to both prevent and reverse the naloxone-induced contraction after exposure to the opioid agonists, in a concentration-dependent fashion. In addition, nordihydroguaiaretic acid (a 5-lipooxygenase inhibitor) was able to block the naloxone-induced contraction following exposure to DAMGO or U50-488H if injected either before or after the opioid agonist. In contrast, mepacrine, tolmetin, meloxicam and nordihydroguaiaretic acid did not affect the naloxone-induced contraction after exposure to deltorphin. The results of the present study confirm and extend a previous study performed with morphine indicating that arachidonic acid and its metabolites (prostaglandins and leukotrienes) are involved in the development of opioid withdrawal induced by selective mu and kappa opioid agonists whereas no effects were observed on withdrawal induced by the selective delta opioid agonist deltorphin.
journal_name
Neuropharmacologyjournal_title
Neuropharmacologyauthors
Capasso Adoi
10.1016/s0028-3908(99)00004-0subject
Has Abstractpub_date
1999-06-01 00:00:00pages
871-7issue
6eissn
0028-3908issn
1873-7064pii
S0028390899000040journal_volume
38pub_type
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