| First Author | Schuller AG | Year | 1999 |
| Journal | Nat Neurosci | Volume | 2 |
| Issue | 2 | Pages | 151-6 |
| PubMed ID | 10195199 | Mgi Jnum | J:52952 |
| Mgi Id | MGI:1330694 | Doi | 10.1038/5706 |
| Citation | Schuller AG, et al. (1999) Retention of heroin and morphine-6 beta-glucuronide analgesia in a new line of mice lacking exon 1 of MOR-1. Nat Neurosci 2(2):151-6 |
| abstractText | 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-l 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. |
