Methadone and Heroin Antinociception: Predominant δ-Opioid-Receptor Responses in Methadone-Tolerant Mice
Antinociceptive tail flick responses to heroin and 6-monoacetylmorphine mediated in the brain by μ-opioid receptor are switched by morphine pellet implantation to δ1-and δ2-opioid-receptors mediation, respectively. Present results showed that the μ-receptor response (inhibited by β-funaltrexamine) t...
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| Veröffentlicht in: | Japanese journal of pharmacology 2002, Vol.88(3), pp.319-331 |
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| creator | Rady, Jodie J. Portoghese, Philip S. Fujimoto, James M. |
| description | Antinociceptive tail flick responses to heroin and 6-monoacetylmorphine mediated in the brain by μ-opioid receptor are switched by morphine pellet implantation to δ1-and δ2-opioid-receptors mediation, respectively. Present results showed that the μ-receptor response (inhibited by β-funaltrexamine) to methadone was changed by morphine pellet implantation to δ1 (inhibited by 7-benzylidenenaltrexone)- and δ2 (inhibited by naltriben)-opioid-receptor responses. Methadone pellet implantation likewise changed mediation from μ- to δ-opioid receptors for heroin and methadone but not for morphine (β-funaltrexamine continued to inhibit). Methadone μ action in the brain was linked through a descending system to activate spinal serotonin receptors (inhibited by methysergide), but this link was gone in the methadone-pellet-implanted group. In the latter group, the new δ1- and δ2-receptor responses were mediated by spinal GABAA (inhibited by bicuculline) and GABAB (inhibited by 2-hydroxysaclofen) receptors. These shifts in neuronal systems meant that μ receptors on a given neuron were not changed into δ receptors. Preliminary results showed that δ-agonist action for methadone was prevented from appearing by MK801, a NMDA-receptor antagonist, and did not occur in 129S6/SvEv mice which lack NMDA responsiveness. Could methadone maintenance treatment in humans uncover δ-agonist actions? |
| doi_str_mv | 10.1254/jjp.88.319 |
| format | Article |
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Present results showed that the μ-receptor response (inhibited by β-funaltrexamine) to methadone was changed by morphine pellet implantation to δ1 (inhibited by 7-benzylidenenaltrexone)- and δ2 (inhibited by naltriben)-opioid-receptor responses. Methadone pellet implantation likewise changed mediation from μ- to δ-opioid receptors for heroin and methadone but not for morphine (β-funaltrexamine continued to inhibit). Methadone μ action in the brain was linked through a descending system to activate spinal serotonin receptors (inhibited by methysergide), but this link was gone in the methadone-pellet-implanted group. In the latter group, the new δ1- and δ2-receptor responses were mediated by spinal GABAA (inhibited by bicuculline) and GABAB (inhibited by 2-hydroxysaclofen) receptors. These shifts in neuronal systems meant that μ receptors on a given neuron were not changed into δ receptors. Preliminary results showed that δ-agonist action for methadone was prevented from appearing by MK801, a NMDA-receptor antagonist, and did not occur in 129S6/SvEv mice which lack NMDA responsiveness. Could methadone maintenance treatment in humans uncover δ-agonist actions?</description><identifier>ISSN: 0021-5198</identifier><identifier>EISSN: 1347-3506</identifier><identifier>DOI: 10.1254/jjp.88.319</identifier><identifier>PMID: 11949888</identifier><language>eng</language><publisher>Japan: The Japanese Pharmacological Society</publisher><subject>Analgesics, Opioid - administration & dosage ; Analgesics, Opioid - pharmacology ; Animals ; Antinociception ; Chronic methadone ; Dose-Response Relationship, Drug ; Drug Implants ; Drug Tolerance ; Heroin ; Heroin - pharmacology ; Injections, Intraventricular ; Methadone ; Methadone - administration & dosage ; Methadone - pharmacology ; Mice ; Receptors, N-Methyl-D-Aspartate - drug effects ; Receptors, Opioid, delta - antagonists & inhibitors ; Receptors, Opioid, delta - drug effects ; Receptors, Opioid, mu - antagonists & inhibitors ; Species Specificity ; δ-Opioid receptor</subject><ispartof>The Japanese Journal of Pharmacology, 2002, Vol.88(3), pp.319-331</ispartof><rights>The Japanese Pharmacological Society 2002</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,1876,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11949888$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Rady, Jodie J.</creatorcontrib><creatorcontrib>Portoghese, Philip S.</creatorcontrib><creatorcontrib>Fujimoto, James M.</creatorcontrib><title>Methadone and Heroin Antinociception: Predominant δ-Opioid-Receptor Responses in Methadone-Tolerant Mice</title><title>Japanese journal of pharmacology</title><addtitle>Jpn.J.Pharmacol.</addtitle><description>Antinociceptive tail flick responses to heroin and 6-monoacetylmorphine mediated in the brain by μ-opioid receptor are switched by morphine pellet implantation to δ1-and δ2-opioid-receptors mediation, respectively. Present results showed that the μ-receptor response (inhibited by β-funaltrexamine) to methadone was changed by morphine pellet implantation to δ1 (inhibited by 7-benzylidenenaltrexone)- and δ2 (inhibited by naltriben)-opioid-receptor responses. Methadone pellet implantation likewise changed mediation from μ- to δ-opioid receptors for heroin and methadone but not for morphine (β-funaltrexamine continued to inhibit). Methadone μ action in the brain was linked through a descending system to activate spinal serotonin receptors (inhibited by methysergide), but this link was gone in the methadone-pellet-implanted group. In the latter group, the new δ1- and δ2-receptor responses were mediated by spinal GABAA (inhibited by bicuculline) and GABAB (inhibited by 2-hydroxysaclofen) receptors. These shifts in neuronal systems meant that μ receptors on a given neuron were not changed into δ receptors. Preliminary results showed that δ-agonist action for methadone was prevented from appearing by MK801, a NMDA-receptor antagonist, and did not occur in 129S6/SvEv mice which lack NMDA responsiveness. Could methadone maintenance treatment in humans uncover δ-agonist actions?</description><subject>Analgesics, Opioid - administration & dosage</subject><subject>Analgesics, Opioid - pharmacology</subject><subject>Animals</subject><subject>Antinociception</subject><subject>Chronic methadone</subject><subject>Dose-Response Relationship, Drug</subject><subject>Drug Implants</subject><subject>Drug Tolerance</subject><subject>Heroin</subject><subject>Heroin - pharmacology</subject><subject>Injections, Intraventricular</subject><subject>Methadone</subject><subject>Methadone - administration & dosage</subject><subject>Methadone - pharmacology</subject><subject>Mice</subject><subject>Receptors, N-Methyl-D-Aspartate - drug effects</subject><subject>Receptors, Opioid, delta - antagonists & inhibitors</subject><subject>Receptors, Opioid, delta - drug effects</subject><subject>Receptors, Opioid, mu - antagonists & inhibitors</subject><subject>Species Specificity</subject><subject>δ-Opioid receptor</subject><issn>0021-5198</issn><issn>1347-3506</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kMFOwkAQhjdGI4hefADTk7fiDtulUy-GEBUTCIbgudm2U9mm7NbdcvC9fA6fyRKQy0wm8_1__vyM3QIfwkhGD1XVDBGHApIz1gcRxaGQfHzO-pyPIJSQYI9deV91J3KILlkPIIkSROwzvaB2owprKFCmCGbkrDbBxLTa2Fzn1LTamsfg3VFht9oo0wa_P-Gy0VYX4Yr2gHXBinxjjScfdOKTY7i2Nbm9ZNE5XbOLUtWebo57wD5entfTWThfvr5NJ_OwEohtFx2wjDBGhYmUlFE2lnEkkogXSFnGpRAxYgmcQ8JlmUMOcR6NIBOFykQmxYDdH3wbZ7925Nt0q31Oda0M2Z1PYxiLGGLegXdHcJdtqUgbp7fKfaf_5XTA0wGofKs-6QQo1-q8prTrPUVMxWF09Z8--Ua5lIz4AzUtffQ</recordid><startdate>20020301</startdate><enddate>20020301</enddate><creator>Rady, Jodie J.</creator><creator>Portoghese, Philip S.</creator><creator>Fujimoto, James M.</creator><general>The Japanese Pharmacological Society</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>20020301</creationdate><title>Methadone and Heroin Antinociception: Predominant δ-Opioid-Receptor Responses in Methadone-Tolerant Mice</title><author>Rady, Jodie J. ; Portoghese, Philip S. ; Fujimoto, James M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-j388t-3518f4878a8955ebeb65743940d8ebb0533788f1001905fc1c17c421b3dab3b53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Analgesics, Opioid - administration & dosage</topic><topic>Analgesics, Opioid - pharmacology</topic><topic>Animals</topic><topic>Antinociception</topic><topic>Chronic methadone</topic><topic>Dose-Response Relationship, Drug</topic><topic>Drug Implants</topic><topic>Drug Tolerance</topic><topic>Heroin</topic><topic>Heroin - pharmacology</topic><topic>Injections, Intraventricular</topic><topic>Methadone</topic><topic>Methadone - administration & dosage</topic><topic>Methadone - pharmacology</topic><topic>Mice</topic><topic>Receptors, N-Methyl-D-Aspartate - drug effects</topic><topic>Receptors, Opioid, delta - antagonists & inhibitors</topic><topic>Receptors, Opioid, delta - drug effects</topic><topic>Receptors, Opioid, mu - antagonists & inhibitors</topic><topic>Species Specificity</topic><topic>δ-Opioid receptor</topic><toplevel>online_resources</toplevel><creatorcontrib>Rady, Jodie J.</creatorcontrib><creatorcontrib>Portoghese, Philip S.</creatorcontrib><creatorcontrib>Fujimoto, James M.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Japanese journal of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Rady, Jodie J.</au><au>Portoghese, Philip S.</au><au>Fujimoto, James M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Methadone and Heroin Antinociception: Predominant δ-Opioid-Receptor Responses in Methadone-Tolerant Mice</atitle><jtitle>Japanese journal of pharmacology</jtitle><addtitle>Jpn.J.Pharmacol.</addtitle><date>2002-03-01</date><risdate>2002</risdate><volume>88</volume><issue>3</issue><spage>319</spage><epage>331</epage><pages>319-331</pages><issn>0021-5198</issn><eissn>1347-3506</eissn><abstract>Antinociceptive tail flick responses to heroin and 6-monoacetylmorphine mediated in the brain by μ-opioid receptor are switched by morphine pellet implantation to δ1-and δ2-opioid-receptors mediation, respectively. Present results showed that the μ-receptor response (inhibited by β-funaltrexamine) to methadone was changed by morphine pellet implantation to δ1 (inhibited by 7-benzylidenenaltrexone)- and δ2 (inhibited by naltriben)-opioid-receptor responses. Methadone pellet implantation likewise changed mediation from μ- to δ-opioid receptors for heroin and methadone but not for morphine (β-funaltrexamine continued to inhibit). Methadone μ action in the brain was linked through a descending system to activate spinal serotonin receptors (inhibited by methysergide), but this link was gone in the methadone-pellet-implanted group. In the latter group, the new δ1- and δ2-receptor responses were mediated by spinal GABAA (inhibited by bicuculline) and GABAB (inhibited by 2-hydroxysaclofen) receptors. These shifts in neuronal systems meant that μ receptors on a given neuron were not changed into δ receptors. Preliminary results showed that δ-agonist action for methadone was prevented from appearing by MK801, a NMDA-receptor antagonist, and did not occur in 129S6/SvEv mice which lack NMDA responsiveness. Could methadone maintenance treatment in humans uncover δ-agonist actions?</abstract><cop>Japan</cop><pub>The Japanese Pharmacological Society</pub><pmid>11949888</pmid><doi>10.1254/jjp.88.319</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Analgesics, Opioid - administration & dosage Analgesics, Opioid - pharmacology Animals Antinociception Chronic methadone Dose-Response Relationship, Drug Drug Implants Drug Tolerance Heroin Heroin - pharmacology Injections, Intraventricular Methadone Methadone - administration & dosage Methadone - pharmacology Mice Receptors, N-Methyl-D-Aspartate - drug effects Receptors, Opioid, delta - antagonists & inhibitors Receptors, Opioid, delta - drug effects Receptors, Opioid, mu - antagonists & inhibitors Species Specificity δ-Opioid receptor |
| title | Methadone and Heroin Antinociception: Predominant δ-Opioid-Receptor Responses in Methadone-Tolerant Mice |
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