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

@article{citeulike:1010130, abstract = {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.}, address = {Dept. of Neuroscience and Cell Biology, UMDNJ-Robert Wood Johnson Medical School, Pisc\"{a}taway 08854, USA.}, author = {Schuller, A. G. and King, M. A. and Zhang, J. and Bolan, E. and Pan, Y. X. and Morgan, D. J. and Chang, A. and Czick, M. E. and Unterwald, E. M. and Pasternak, G. W. and Pintar, J. E.}, citeulike-article-id = {1010130}, citeulike-linkout-0 = {http://dx.doi.org/10.1038/5706}, citeulike-linkout-1 = {http://view.ncbi.nlm.nih.gov/pubmed/10195199}, citeulike-linkout-2 = {http://www.hubmed.org/display.cgi?uids=10195199}, doi = {10.1038/5706}, issn = {1097-6256}, journal = {Nat Neurosci}, keywords = {analgesia, beta-glucuronide, heroin, mor-1, morphine, morphine-6, opiate, opioid}, month = {February}, number = {2}, pages = {151--156}, posted-at = {2006-12-23 00:47:35}, priority = {0}, title = {Retention of heroin and morphine-6 beta-glucuronide analgesia in a new line of mice lacking exon 1 of MOR-1.}, url = {http://dx.doi.org/10.1038/5706}, volume = {2}, year = {1999} }

TY - JOUR ID - citeulike:1010130 L3 - citeulike-article-id:1010130 N2 - 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. IS - 2 JF - Nat Neurosci SN - 1097-6256 AD - Dept. of Neuroscience and Cell Biology, UMDNJ-Robert Wood Johnson Medical School, Piscätaway 08854, USA. EP - 156 TI - Retention of heroin and morphine-6 beta-glucuronide analgesia in a new line of mice lacking exon 1 of MOR-1. VL - 2 SP - 151 KW - analgesia KW - beta-glucuronide KW - heroin KW - mor-1 KW - morphine KW - morphine-6 KW - opiate KW - opioid AU - Schuller, AG AU - King, MA AU - Zhang, J AU - Bolan, E AU - Pan, YX AU - Morgan, DJ AU - Chang, A AU - Czick, ME AU - Unterwald, EM AU - Pasternak, GW AU - Pintar, JE PY - 1999/02// UR - http://dx.doi.org/10.1038/5706 ER -