mu opiate receptor: cDNA cloning and expression.

Wang, Jia Bei; Imai, Yasuo; Eppler, C M; Gregor, Paul; Spivak, Charles E.; Uhl, George R.

doi:10.1073/pnas.90.21.10230

Cited by 362 publications

(189 citation statements)

References 60 publications

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“…1B), the secretion signal of the S. cerevisiae c~-mating factor was used to facilitate membrane translocation of the receptor. In both cases, part of the amino-terminus of the receptor was deleted since it has been reported that this had no effect on ligand binding [20][21][22]. DNA fragments comprising the fusion genes flanked by 5' and 3' AOX1 sequences were electro-transformed into the GSll5 (his4) and the protease-deficient SMDl168 (his4, pep4) P. pastoris strains and His + transformants were selected.…”

Section: Resultsmentioning

confidence: 99%

Expression and pharmacological characterization of the human μ‐opioid receptor in the methylotrophic yeast Pichia pastoris

et al. 1996

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Section: Resultsmentioning

confidence: 99%

Expression and pharmacological characterization of the human μ‐opioid receptor in the methylotrophic yeast Pichia pastoris

et al. 1996

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“…Morphine acts at seven transmembrane domain, G proteinlinked receptor products of genes encoding , , and ␦ opiate receptor subtypes (1)(2)(3)(4)(5)(6)(7)(8)(9). Each of these genes is expressed in neurons in several neuronal circuits implicated in nociception (10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20).…”

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confidence: 99%

Opiate receptor knockout mice define μ receptor roles in endogenous nociceptive responses and morphine-induced analgesia

Sora

Takahashi

Funada

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

476

335

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Morphine produces analgesia at opiate receptors expressed in nociceptive circuits. , ␦, and opiate receptor subtypes are expressed in circuits that can modulate nociception and receive inputs from endogenous opioid neuropeptide ligands. The roles played by each receptor subtype in nociceptive processing in drug-free and morphine-treated states have not been clear, however. We produced homologous, recombinant , opiate receptor, heterozygous and homozygous knockout animals that displayed Ϸ54% and 0% of wild-type levels of receptor expression, respectively. These mice expressed receptors and ␦ receptors at near wild-type levels. Untreated knockout mice displayed shorter latencies on tail f lick and hot plate tests for spinal and supraspinal nociceptive responses than wild-type mice. These findings support a significant role for endogenous opioid-peptide interactions with opiate receptors in normal nociceptive processing. Morphine failed to significantly reduce nociceptive responses in hot plate or tail f lick tests of homozygous receptor knockout mice, and heterozygote mice displayed right and downward shifts in morphine analgesia dose-effect relationships. These results implicate endogenous opioidpeptide actions at opiate receptors in several tests of nociceptive responsiveness and support receptor mediation of morphine-induced analgesia in tests of spinal and supraspinal analgesia.Morphine acts at seven transmembrane domain, G proteinlinked receptor products of genes encoding , , and ␦ opiate receptor subtypes (1-9). Each of these genes is expressed in neurons in several neuronal circuits implicated in nociception (10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20).receptor mediation of much morphine-induced analgesia has been postulated (21, 22). However, studies using compounds with relative preferences for ␦ and receptors have suggested that these other two opiate receptor subtypes also might play significant roles in the analgesic responses induced by morphine-like drugs (22-26). The extent to which each of the three opiate receptor subtype gene products might participate in different features of opiate-or morphineinduced analgesia thus has remained unclear. Elucidation of the selective analgesic contributions of each opiate receptor subtype is of substantial potential importance for developing improved analgesic medications with minimal undesirable effects.Expression of endogenous opioid-peptide agonists, especially those derived from the preproenkephalin and preprodynorphin genes, in circuits associated with pain perception suggests that opioid-peptide interactions with opiate receptors could be well positioned to modulate nociceptive responses in the absence of exogenously administered opiate drugs (10,12,14,(27)(28)(29)(30)(31)(32). Studies of pain responses in animals and humans treated with opiate antagonists, however, have documented modifications in nociception in some but not all studies (33,34). These results also have left uncertainty about the power of endogenous opioid-peptide interactions with ...

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“…The -opioid receptor ( OR) is a seven-transmembrane domain, G protein-linked receptor that is a key member (Wang et al 1993), along with the enkephalinpreferring ␦ (Kieffer et al 1992) and dynorphin-preferring receptors (Minami et al 1993), of the constellation of brain receptors that recognize morphine and other opiate drugs (Uhl et al 1994). Pharmacologic approaches have suggested that the receptor, for which morphine has the highest affinity (Pasternak 1993), also serves as a principal site for morphine actions in inducing behavioral reward (Di Chiara and North 1992;Wise 1996), locomotion (Stevens et al 1986), analgesia (Porreca and Burks 1993), tolerance (Aghajanian 1978), and physical dependence (Johnson and Fleming 1989).…”

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confidence: 99%

μ Opiate Receptor Gene Dose Effects on Different Morphine Actions Evidence for Differential in vivo μ Receptor Reserve

Sora¹,

Elmer

Funada

et al. 2001

Neuropsychopharmacology

133

118

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mu opiate receptor: cDNA cloning and expression.

Cited by 362 publications

References 60 publications

Expression and pharmacological characterization of the human μ‐opioid receptor in the methylotrophic yeast Pichia pastoris

Expression and pharmacological characterization of the human μ‐opioid receptor in the methylotrophic yeast Pichia pastoris

Opiate receptor knockout mice define μ receptor roles in endogenous nociceptive responses and morphine-induced analgesia

μ Opiate Receptor Gene Dose Effects on Different Morphine Actions Evidence for Differential in vivo μ Receptor Reserve

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