beta-Funaltrexamine inactivates ORL1 receptors in BE(2)-C human neuroblastoma cells

Eur J Pharmacol. 2000 Aug 18;402(1-2):R1-37. doi: 10.1016/s0014-2999(00)00497-0.

Abstract

The potential interactions of natively expressed mu-opioid and opioid receptor-like (ORL1) receptors were studied by exposing intact BE(2)-C cells to agonists or antagonists for 1 h. Pretreatment with the mu-opioid receptor agonist, [D-Ala(2), N-Me-Phe(4),Gly(5)-ol]enkephalin (DAMGO), or the ORL1 receptor agonist, orphanin FQ/nociceptin desensitized both mu-opioid and ORL1 receptor responses. beta-Funaltrexamine (beta-FNA) pretreatment also blocked both mu-opioid and ORL1 receptor responses, but only mu-opioid receptor binding was reduced. Moreover, beta-FNA (1 microM) failed to inhibit specific ORL1 receptor binding.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Brain Neoplasms / metabolism*
  • Cyclic AMP / metabolism
  • Enkephalin, Ala(2)-MePhe(4)-Gly(5)- / metabolism
  • Humans
  • Morphine / pharmacology
  • Naltrexone / analogs & derivatives*
  • Naltrexone / pharmacology
  • Narcotic Antagonists* / pharmacology*
  • Narcotics / pharmacology
  • Neuroblastoma / metabolism*
  • Opioid Peptides / pharmacology
  • Receptors, Opioid / agonists
  • Receptors, Opioid, mu / antagonists & inhibitors
  • Tumor Cells, Cultured

Substances

  • Narcotic Antagonists
  • Narcotics
  • Opioid Peptides
  • Receptors, Opioid
  • Receptors, Opioid, mu
  • Enkephalin, Ala(2)-MePhe(4)-Gly(5)-
  • Naltrexone
  • beta-funaltrexamine
  • Morphine
  • nociceptin
  • nociceptin receptor
  • Cyclic AMP