Antagonistic property of buprenorphine for putative ϵ-opioid receptor-mediated G-protein activation by β-endorphin in pons/medulla of the μ-opioid receptor knockout mouse
β-Endorphin is a non-selective opioid peptide which binds μ-, δ- and putative ϵ (β-endorphin-sensitive non-μ-, non-δ- and non-κ 1-)-opioid receptors. We have previously reported that β-endorphin-produced G-protein activation is mediated by the stimulation of both μ- and putative ϵ-opioid receptors....
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| creator | Mizoguchi, H Wu, H.-E Narita, M Hall, F.S Sora, I Uhl, G.R Nagase, H Tseng, L.F |
| description | β-Endorphin is a non-selective opioid peptide which binds μ-, δ- and putative ϵ (β-endorphin-sensitive non-μ-, non-δ- and non-κ
1-)-opioid receptors. We have previously reported that β-endorphin-produced G-protein activation is mediated by the stimulation of both μ- and putative ϵ-opioid receptors. The present study was designed to further characterize this putative ϵ-opioid receptor-mediated G-protein activation in the pons/medulla membrane obtained from mice lacking μ-opioid receptor, using a guanosine-5′-
O-(3-[
35S]thio)triphosphate ([
35S]GTPγS)-binding assay. β-Endorphin and the μ-opioid receptor agonist [
D-Ala
2,N-MePhe
4,Gly-ol
5]enkephalin (DAMGO) increased the [
35S]GTPγS binding in a concentration-dependent manner (0.001–10 μM), and at 10 μM β-endorphin and DAMGO produced approximately 250 and 120% increases of [
35S]GTPγS binding in the pons/medulla membrane obtained from wild-type mice, respectively. In the pons/medulla membrane obtained from μ-opioid receptor knockout mice, β-endorphin-stimulated [
35S]GTPγS binding was only partially attenuated and a more than 100% increase by 10 μM β-endorphin still remained, while DAMGO failed to produce any increase in [
35S]GTPγS binding. The residual increase in [
35S]GTPγS binding by 10 μM β-endorphin in μ-opioid receptor knockout mice was partially but significantly attenuated by the putative ϵ-opioid receptor partial agonist β-endorphin (1–27), but not by the δ-opioid receptor antagonist naltrindole or the κ
1-receptor antagonist norbinaltorphimine. Furthermore, buprenorphine significantly attenuated the residual increase in [
35S]GTPγS binding by 10 μM β-endorphin in μ-opioid receptor knockout mice. The present results indicate that β-endorphin activates G-protein by stimulation of putative ϵ-opioid receptors in the condition lacking the μ-opioid receptor, and buprenorphine acts as an antagonist for putative ϵ-opioid receptors in this condition. |
| doi_str_mv | 10.1016/S0306-4522(02)00486-4 |
| format | Article |
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1-)-opioid receptors. We have previously reported that β-endorphin-produced G-protein activation is mediated by the stimulation of both μ- and putative ϵ-opioid receptors. The present study was designed to further characterize this putative ϵ-opioid receptor-mediated G-protein activation in the pons/medulla membrane obtained from mice lacking μ-opioid receptor, using a guanosine-5′-
O-(3-[
35S]thio)triphosphate ([
35S]GTPγS)-binding assay. β-Endorphin and the μ-opioid receptor agonist [
D-Ala
2,N-MePhe
4,Gly-ol
5]enkephalin (DAMGO) increased the [
35S]GTPγS binding in a concentration-dependent manner (0.001–10 μM), and at 10 μM β-endorphin and DAMGO produced approximately 250 and 120% increases of [
35S]GTPγS binding in the pons/medulla membrane obtained from wild-type mice, respectively. In the pons/medulla membrane obtained from μ-opioid receptor knockout mice, β-endorphin-stimulated [
35S]GTPγS binding was only partially attenuated and a more than 100% increase by 10 μM β-endorphin still remained, while DAMGO failed to produce any increase in [
35S]GTPγS binding. The residual increase in [
35S]GTPγS binding by 10 μM β-endorphin in μ-opioid receptor knockout mice was partially but significantly attenuated by the putative ϵ-opioid receptor partial agonist β-endorphin (1–27), but not by the δ-opioid receptor antagonist naltrindole or the κ
1-receptor antagonist norbinaltorphimine. Furthermore, buprenorphine significantly attenuated the residual increase in [
35S]GTPγS binding by 10 μM β-endorphin in μ-opioid receptor knockout mice. The present results indicate that β-endorphin activates G-protein by stimulation of putative ϵ-opioid receptors in the condition lacking the μ-opioid receptor, and buprenorphine acts as an antagonist for putative ϵ-opioid receptors in this condition.</description><identifier>ISSN: 0306-4522</identifier><identifier>EISSN: 1873-7544</identifier><identifier>DOI: 10.1016/S0306-4522(02)00486-4</identifier><identifier>PMID: 12435410</identifier><identifier>CODEN: NRSCDN</identifier><language>eng</language><publisher>Oxford: Elsevier Ltd</publisher><subject>Animals ; antagonist ; beta-Endorphin - antagonists & inhibitors ; beta-Endorphin - metabolism ; Binding, Competitive - drug effects ; Binding, Competitive - physiology ; Biological and medical sciences ; Buprenorphine - pharmacology ; Cell Membrane - drug effects ; Cell Membrane - metabolism ; Central nervous system ; Central neurotransmission. Neuromudulation. Pathways and receptors ; Enkephalin, Ala-MePhe-Gly- - pharmacology ; Female ; Fundamental and applied biological sciences. Psychology ; GTP-Binding Proteins - drug effects ; GTP-Binding Proteins - metabolism ; Guanosine 5'-O-(3-Thiotriphosphate) ; guanosine-5′- O-(3-[ 35S]thio)triphosphate binding ; Male ; Medulla Oblongata - drug effects ; Medulla Oblongata - metabolism ; Mice ; Mice, Knockout ; Naltrexone - analogs & derivatives ; Naltrexone - pharmacology ; Narcotic Antagonists ; Narcotics - pharmacology ; Neurons - drug effects ; Neurons - metabolism ; Peptide Fragments - pharmacology ; Pons - drug effects ; Pons - metabolism ; Radioligand Assay ; Receptors, Opioid - metabolism ; Receptors, Opioid, mu - deficiency ; Receptors, Opioid, mu - drug effects ; Receptors, Opioid, mu - genetics ; Rhombencephalon - drug effects ; Rhombencephalon - metabolism ; Sulfur Radioisotopes ; Synaptic Transmission - drug effects ; Synaptic Transmission - physiology ; Vertebrates: nervous system and sense organs</subject><ispartof>Neuroscience, 2002-01, Vol.115 (3), p.715-721</ispartof><rights>2002 IBRO</rights><rights>2003 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c391t-556fac79ffe55e4067efe9af1e356fd8406ec51dbd1deded8c049f1695ebbbd23</citedby><cites>FETCH-LOGICAL-c391t-556fac79ffe55e4067efe9af1e356fd8406ec51dbd1deded8c049f1695ebbbd23</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S0306-4522(02)00486-4$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,778,782,3539,27907,27908,45978</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14012462$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12435410$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mizoguchi, H</creatorcontrib><creatorcontrib>Wu, H.-E</creatorcontrib><creatorcontrib>Narita, M</creatorcontrib><creatorcontrib>Hall, F.S</creatorcontrib><creatorcontrib>Sora, I</creatorcontrib><creatorcontrib>Uhl, G.R</creatorcontrib><creatorcontrib>Nagase, H</creatorcontrib><creatorcontrib>Tseng, L.F</creatorcontrib><title>Antagonistic property of buprenorphine for putative ϵ-opioid receptor-mediated G-protein activation by β-endorphin in pons/medulla of the μ-opioid receptor knockout mouse</title><title>Neuroscience</title><addtitle>Neuroscience</addtitle><description>β-Endorphin is a non-selective opioid peptide which binds μ-, δ- and putative ϵ (β-endorphin-sensitive non-μ-, non-δ- and non-κ
1-)-opioid receptors. We have previously reported that β-endorphin-produced G-protein activation is mediated by the stimulation of both μ- and putative ϵ-opioid receptors. The present study was designed to further characterize this putative ϵ-opioid receptor-mediated G-protein activation in the pons/medulla membrane obtained from mice lacking μ-opioid receptor, using a guanosine-5′-
O-(3-[
35S]thio)triphosphate ([
35S]GTPγS)-binding assay. β-Endorphin and the μ-opioid receptor agonist [
D-Ala
2,N-MePhe
4,Gly-ol
5]enkephalin (DAMGO) increased the [
35S]GTPγS binding in a concentration-dependent manner (0.001–10 μM), and at 10 μM β-endorphin and DAMGO produced approximately 250 and 120% increases of [
35S]GTPγS binding in the pons/medulla membrane obtained from wild-type mice, respectively. In the pons/medulla membrane obtained from μ-opioid receptor knockout mice, β-endorphin-stimulated [
35S]GTPγS binding was only partially attenuated and a more than 100% increase by 10 μM β-endorphin still remained, while DAMGO failed to produce any increase in [
35S]GTPγS binding. The residual increase in [
35S]GTPγS binding by 10 μM β-endorphin in μ-opioid receptor knockout mice was partially but significantly attenuated by the putative ϵ-opioid receptor partial agonist β-endorphin (1–27), but not by the δ-opioid receptor antagonist naltrindole or the κ
1-receptor antagonist norbinaltorphimine. Furthermore, buprenorphine significantly attenuated the residual increase in [
35S]GTPγS binding by 10 μM β-endorphin in μ-opioid receptor knockout mice. The present results indicate that β-endorphin activates G-protein by stimulation of putative ϵ-opioid receptors in the condition lacking the μ-opioid receptor, and buprenorphine acts as an antagonist for putative ϵ-opioid receptors in this condition.</description><subject>Animals</subject><subject>antagonist</subject><subject>beta-Endorphin - antagonists & inhibitors</subject><subject>beta-Endorphin - metabolism</subject><subject>Binding, Competitive - drug effects</subject><subject>Binding, Competitive - physiology</subject><subject>Biological and medical sciences</subject><subject>Buprenorphine - pharmacology</subject><subject>Cell Membrane - drug effects</subject><subject>Cell Membrane - metabolism</subject><subject>Central nervous system</subject><subject>Central neurotransmission. Neuromudulation. Pathways and receptors</subject><subject>Enkephalin, Ala-MePhe-Gly- - pharmacology</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>GTP-Binding Proteins - drug effects</subject><subject>GTP-Binding Proteins - metabolism</subject><subject>Guanosine 5'-O-(3-Thiotriphosphate)</subject><subject>guanosine-5′- O-(3-[ 35S]thio)triphosphate binding</subject><subject>Male</subject><subject>Medulla Oblongata - drug effects</subject><subject>Medulla Oblongata - metabolism</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Naltrexone - analogs & derivatives</subject><subject>Naltrexone - pharmacology</subject><subject>Narcotic Antagonists</subject><subject>Narcotics - pharmacology</subject><subject>Neurons - drug effects</subject><subject>Neurons - metabolism</subject><subject>Peptide Fragments - pharmacology</subject><subject>Pons - drug effects</subject><subject>Pons - metabolism</subject><subject>Radioligand Assay</subject><subject>Receptors, Opioid - metabolism</subject><subject>Receptors, Opioid, mu - deficiency</subject><subject>Receptors, Opioid, mu - drug effects</subject><subject>Receptors, Opioid, mu - genetics</subject><subject>Rhombencephalon - drug effects</subject><subject>Rhombencephalon - metabolism</subject><subject>Sulfur Radioisotopes</subject><subject>Synaptic Transmission - drug effects</subject><subject>Synaptic Transmission - physiology</subject><subject>Vertebrates: nervous system and sense organs</subject><issn>0306-4522</issn><issn>1873-7544</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc9uFSEUxomxsdfqI2jYaHQxLczA_FmZptFq0qQLdU0YOFjsvTAC0-Q-lBsTdz5DfSXPeG_axI1AQoDfd87hfIQ84-yYM96efGQNaysh6_oVq18zJno8PSAr3ndN1UkhHpLVHXJIHuf8leGQonlEDnktGik4W5Hvp6HoLzH4XLyhU4oTpLKl0dFxnhKEmKYrH4C6mOg0F138DdDfP6s4-egtTWBgKjFVG7BeF7D0vMIgBXyg2iCMghjouKW3PyoIdheO4ppiyCeomtdrvaQrV0Bvf_0bl16HaK7jXOgmzhmekAOn1xme7vcj8vnd209n76uLy_MPZ6cXlWkGXiopW6dNNzgHUoJgbQcOBu04NPhie7wBI7kdLbeAszdMDI63g4RxHG3dHJGXu7j4l28z5KI2PhvAUgNgHaqr276tB4mg3IEmxZwTODUlv9FpqzhTi0_qr09qMUExXItPSqDu-T7BPGIT7lV7YxB4sQd0Nnrtkg7G53tOMETbpdI3Ow6wHTceksrGQzBoB_awKBv9f0r5AxQEt5A</recordid><startdate>20020101</startdate><enddate>20020101</enddate><creator>Mizoguchi, H</creator><creator>Wu, H.-E</creator><creator>Narita, M</creator><creator>Hall, F.S</creator><creator>Sora, I</creator><creator>Uhl, G.R</creator><creator>Nagase, H</creator><creator>Tseng, L.F</creator><general>Elsevier Ltd</general><general>Elsevier</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20020101</creationdate><title>Antagonistic property of buprenorphine for putative ϵ-opioid receptor-mediated G-protein activation by β-endorphin in pons/medulla of the μ-opioid receptor knockout mouse</title><author>Mizoguchi, H ; Wu, H.-E ; Narita, M ; Hall, F.S ; Sora, I ; Uhl, G.R ; Nagase, H ; Tseng, L.F</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c391t-556fac79ffe55e4067efe9af1e356fd8406ec51dbd1deded8c049f1695ebbbd23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Animals</topic><topic>antagonist</topic><topic>beta-Endorphin - antagonists & inhibitors</topic><topic>beta-Endorphin - metabolism</topic><topic>Binding, Competitive - drug effects</topic><topic>Binding, Competitive - physiology</topic><topic>Biological and medical sciences</topic><topic>Buprenorphine - pharmacology</topic><topic>Cell Membrane - drug effects</topic><topic>Cell Membrane - metabolism</topic><topic>Central nervous system</topic><topic>Central neurotransmission. Neuromudulation. Pathways and receptors</topic><topic>Enkephalin, Ala-MePhe-Gly- - pharmacology</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>GTP-Binding Proteins - drug effects</topic><topic>GTP-Binding Proteins - metabolism</topic><topic>Guanosine 5'-O-(3-Thiotriphosphate)</topic><topic>guanosine-5′- O-(3-[ 35S]thio)triphosphate binding</topic><topic>Male</topic><topic>Medulla Oblongata - drug effects</topic><topic>Medulla Oblongata - metabolism</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Naltrexone - analogs & derivatives</topic><topic>Naltrexone - pharmacology</topic><topic>Narcotic Antagonists</topic><topic>Narcotics - pharmacology</topic><topic>Neurons - drug effects</topic><topic>Neurons - metabolism</topic><topic>Peptide Fragments - pharmacology</topic><topic>Pons - drug effects</topic><topic>Pons - metabolism</topic><topic>Radioligand Assay</topic><topic>Receptors, Opioid - metabolism</topic><topic>Receptors, Opioid, mu - deficiency</topic><topic>Receptors, Opioid, mu - drug effects</topic><topic>Receptors, Opioid, mu - genetics</topic><topic>Rhombencephalon - drug effects</topic><topic>Rhombencephalon - metabolism</topic><topic>Sulfur Radioisotopes</topic><topic>Synaptic Transmission - drug effects</topic><topic>Synaptic Transmission - physiology</topic><topic>Vertebrates: nervous system and sense organs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Mizoguchi, H</creatorcontrib><creatorcontrib>Wu, H.-E</creatorcontrib><creatorcontrib>Narita, M</creatorcontrib><creatorcontrib>Hall, F.S</creatorcontrib><creatorcontrib>Sora, I</creatorcontrib><creatorcontrib>Uhl, G.R</creatorcontrib><creatorcontrib>Nagase, H</creatorcontrib><creatorcontrib>Tseng, L.F</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Mizoguchi, H</au><au>Wu, H.-E</au><au>Narita, M</au><au>Hall, F.S</au><au>Sora, I</au><au>Uhl, G.R</au><au>Nagase, H</au><au>Tseng, L.F</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Antagonistic property of buprenorphine for putative ϵ-opioid receptor-mediated G-protein activation by β-endorphin in pons/medulla of the μ-opioid receptor knockout mouse</atitle><jtitle>Neuroscience</jtitle><addtitle>Neuroscience</addtitle><date>2002-01-01</date><risdate>2002</risdate><volume>115</volume><issue>3</issue><spage>715</spage><epage>721</epage><pages>715-721</pages><issn>0306-4522</issn><eissn>1873-7544</eissn><coden>NRSCDN</coden><abstract>β-Endorphin is a non-selective opioid peptide which binds μ-, δ- and putative ϵ (β-endorphin-sensitive non-μ-, non-δ- and non-κ
1-)-opioid receptors. We have previously reported that β-endorphin-produced G-protein activation is mediated by the stimulation of both μ- and putative ϵ-opioid receptors. The present study was designed to further characterize this putative ϵ-opioid receptor-mediated G-protein activation in the pons/medulla membrane obtained from mice lacking μ-opioid receptor, using a guanosine-5′-
O-(3-[
35S]thio)triphosphate ([
35S]GTPγS)-binding assay. β-Endorphin and the μ-opioid receptor agonist [
D-Ala
2,N-MePhe
4,Gly-ol
5]enkephalin (DAMGO) increased the [
35S]GTPγS binding in a concentration-dependent manner (0.001–10 μM), and at 10 μM β-endorphin and DAMGO produced approximately 250 and 120% increases of [
35S]GTPγS binding in the pons/medulla membrane obtained from wild-type mice, respectively. In the pons/medulla membrane obtained from μ-opioid receptor knockout mice, β-endorphin-stimulated [
35S]GTPγS binding was only partially attenuated and a more than 100% increase by 10 μM β-endorphin still remained, while DAMGO failed to produce any increase in [
35S]GTPγS binding. The residual increase in [
35S]GTPγS binding by 10 μM β-endorphin in μ-opioid receptor knockout mice was partially but significantly attenuated by the putative ϵ-opioid receptor partial agonist β-endorphin (1–27), but not by the δ-opioid receptor antagonist naltrindole or the κ
1-receptor antagonist norbinaltorphimine. Furthermore, buprenorphine significantly attenuated the residual increase in [
35S]GTPγS binding by 10 μM β-endorphin in μ-opioid receptor knockout mice. The present results indicate that β-endorphin activates G-protein by stimulation of putative ϵ-opioid receptors in the condition lacking the μ-opioid receptor, and buprenorphine acts as an antagonist for putative ϵ-opioid receptors in this condition.</abstract><cop>Oxford</cop><pub>Elsevier Ltd</pub><pmid>12435410</pmid><doi>10.1016/S0306-4522(02)00486-4</doi><tpages>7</tpages></addata></record> |
| fulltext | fulltext |
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| ispartof | Neuroscience, 2002-01, Vol.115 (3), p.715-721 |
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| language | eng |
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| source | Elsevier ScienceDirect Journals Complete - AutoHoldings; MEDLINE |
| subjects | Animals antagonist beta-Endorphin - antagonists & inhibitors beta-Endorphin - metabolism Binding, Competitive - drug effects Binding, Competitive - physiology Biological and medical sciences Buprenorphine - pharmacology Cell Membrane - drug effects Cell Membrane - metabolism Central nervous system Central neurotransmission. Neuromudulation. Pathways and receptors Enkephalin, Ala-MePhe-Gly- - pharmacology Female Fundamental and applied biological sciences. Psychology GTP-Binding Proteins - drug effects GTP-Binding Proteins - metabolism Guanosine 5'-O-(3-Thiotriphosphate) guanosine-5′- O-(3-[ 35S]thio)triphosphate binding Male Medulla Oblongata - drug effects Medulla Oblongata - metabolism Mice Mice, Knockout Naltrexone - analogs & derivatives Naltrexone - pharmacology Narcotic Antagonists Narcotics - pharmacology Neurons - drug effects Neurons - metabolism Peptide Fragments - pharmacology Pons - drug effects Pons - metabolism Radioligand Assay Receptors, Opioid - metabolism Receptors, Opioid, mu - deficiency Receptors, Opioid, mu - drug effects Receptors, Opioid, mu - genetics Rhombencephalon - drug effects Rhombencephalon - metabolism Sulfur Radioisotopes Synaptic Transmission - drug effects Synaptic Transmission - physiology Vertebrates: nervous system and sense organs |
| title | Antagonistic property of buprenorphine for putative ϵ-opioid receptor-mediated G-protein activation by β-endorphin in pons/medulla of the μ-opioid receptor knockout mouse |
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