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
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Brain Neoplasms / metabolism*
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Cyclic AMP / metabolism
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Enkephalin, Ala(2)-MePhe(4)-Gly(5)- / metabolism
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Humans
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Morphine / pharmacology
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Naltrexone / analogs & derivatives*
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Naltrexone / pharmacology
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Narcotic Antagonists* / pharmacology*
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Narcotics / pharmacology
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Neuroblastoma / metabolism*
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Nociceptin
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Nociceptin Receptor
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Opioid Peptides / pharmacology
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Receptors, Opioid / agonists
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Receptors, Opioid, mu / antagonists & inhibitors
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Tumor Cells, Cultured
Substances
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Narcotic Antagonists
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Narcotics
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Opioid Peptides
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Receptors, Opioid
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Receptors, Opioid, mu
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Enkephalin, Ala(2)-MePhe(4)-Gly(5)-
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Naltrexone
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beta-funaltrexamine
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Morphine
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Cyclic AMP
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Nociceptin Receptor
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OPRL1 protein, human