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Retention of heroin and morphine-6 beta-glucuronide analgesia in a new line of mice lacking exon 1 of MOR-1.

Morphine produces analgesia by activating mu opioid receptors encoded by the MOR-1 gene. Although morphine-6 beta-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.

Pubmed ID: 10195199

Authors

  • Schuller AG
  • King MA
  • Zhang J
  • Bolan E
  • Pan YX
  • Morgan DJ
  • Chang A
  • Czick ME
  • Unterwald EM
  • Pasternak GW
  • Pintar JE

Journal

Nature neuroscience

Publication Data

February 29, 1999

Associated Grants

  • Agency: NIDA NIH HHS, Id: DA-00296
  • Agency: NIDA NIH HHS, Id: DA-08622
  • Agency: NIDA NIH HHS, Id: DA-09040
  • Agency: NIDA NIH HHS, Id: K01 DA000296
  • Agency: NIDA NIH HHS, Id: R01 DA007242
  • Agency: NIDA NIH HHS, Id: R56 DA002615

Mesh Terms

  • Analgesics, Opioid
  • Animals
  • Drug Resistance
  • Exons
  • Heroin
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Morphine Derivatives
  • Receptors, Opioid, mu
  • Transcription, Genetic