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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.

Nature neuroscience | Feb 29, 1999

http://www.ncbi.nlm.nih.gov/pubmed/10195199

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 RIS Download

Mesh terms: Analgesics, Opioid | Animals | Drug Resistance | Exons | Heroin | Mice | Mice, Inbred C57BL | Mice, Knockout | Morphine Derivatives | Receptors, Opioid, mu | Transcription, Genetic

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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

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