Retention of heroin and morphine-6β-glucuronide analgesia in a new line of mice lacking exon 1 of MOR-1 Journal Article


Authors: Schuller, A. G. P.; King, M. A.; Zhang, J.; Bolan, E.; Pan, Y. X.; Morgan, D. J.; Chang, A.; Czick, M. E.; Unterwald, E. M.; Pasternak, G. W.; Pintar, J. E.
Article Title: Retention of heroin and morphine-6β-glucuronide analgesia in a new line of mice lacking exon 1 of MOR-1
Abstract: Morphine produces analgesia by activating mu opioid receptors encoded by the MOR-1 gene. Although morphine-6β-glucuronide (M6G), heroin and 6- acetylmorphine also are considered mu opioids, recent evidence suggests that they act through a distinct receptor mechanism. We examined this question in knockout mice containing disruptions of either the first or second coding exon of MOR-1. Mice homozygous for either MOR-1 mutation were insensitive to morphine. Heroin, 6-acetylmorphine and M6G still elicited analgesia in the exon-1 MOR-1 mutant, which also showed specific M6G binding, whereas M6G and 6-acetylmorphine were inactive in the exon-2 MOR-1 mutant. These results provide genetic evidence for a unique receptor site for M6G and heroin analgesia.
Keywords: protein expression; exon; exons; nonhuman; animal cell; mouse; animals; mice; mice, knockout; pain; transcription, genetic; drug resistance; mice, inbred c57bl; drug receptor binding; morphine; analgesics, opioid; analgesia; receptors, opioid, mu; diamorphine; morphine 6 glucuronide; heroin; morphine derivatives; priority journal; article
Journal Title: Nature Neuroscience
Volume: 2
Issue: 2
ISSN: 1097-6256
Publisher: Nature Publishing Group  
Date Published: 1999-02-01
Start Page: 151
End Page: 156
Language: English
DOI: 10.1038/5706
PUBMED: 10195199
PROVIDER: scopus
DOI/URL:
Notes: Article -- Export Date: 16 August 2016 -- Source: Scopus
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MSK Authors
  1. Elizabeth A Bolan
    18 Bolan
  2. Michael A King
    24 King
  3. Yingxian Pan
    132 Pan
  4. Gavril W Pasternak
    414 Pasternak
  5. Albert H Chang
    19 Chang