Acute tolerance associated with a single opiate administration: involvement of N-methyl- d-aspartate-dependent pain facilitatory systems
Mechanisms underlying the development of acute tolerance to the analgesic effect of opiates were investigated. In the rat tail-flick test, administration of naloxone (1 mg/kg, s.c.) 40 min after heroin (1 mg/kg, s.c.) was shown to induce hyperalgesia, indicative of a short-onset, opiate-activated pa...
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| Veröffentlicht in: | Neuroscience 1998-05, Vol.84 (2), p.583-589 |
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| creator | Larcher, A Laulin, J.P Celerier, E Le Moal, M Simonnet, G |
| description | Mechanisms underlying the development of acute tolerance to the analgesic effect of opiates were investigated. In the rat tail-flick test, administration of naloxone (1
mg/kg, s.c.) 40
min after heroin (1
mg/kg, s.c.) was shown to induce hyperalgesia, indicative of a short-onset, opiate-activated pain facilitatory systems masking the opiate analgesia. Pretreatment with the
N-methyl-
d-aspartate receptor antagonist dizocilpine maleate blocked, in a dose-dependent manner, the naloxone-induced hyperalgesia and potentiated the heroin-induced analgesia. Using a schedule of two successive injections of 1
mg/kg heroin, acute tolerance was indicated by a marked reduction (−52%) in analgesia induced by the second dose. After pretreatment with dizocilpine maleate, the acute tolerance was abolished and the analgesic effects of both injections of heroin were strongly potentiated.
These observations indicate that acute tolerance appears after the first exposure to opiates and stems from opiate activation of
N-methyl-
d-aspartate-dependent pain facilitatory systems. |
| doi_str_mv | 10.1016/S0306-4522(97)00556-3 |
| format | Article |
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mg/kg, s.c.) 40
min after heroin (1
mg/kg, s.c.) was shown to induce hyperalgesia, indicative of a short-onset, opiate-activated pain facilitatory systems masking the opiate analgesia. Pretreatment with the
N-methyl-
d-aspartate receptor antagonist dizocilpine maleate blocked, in a dose-dependent manner, the naloxone-induced hyperalgesia and potentiated the heroin-induced analgesia. Using a schedule of two successive injections of 1
mg/kg heroin, acute tolerance was indicated by a marked reduction (−52%) in analgesia induced by the second dose. After pretreatment with dizocilpine maleate, the acute tolerance was abolished and the analgesic effects of both injections of heroin were strongly potentiated.
These observations indicate that acute tolerance appears after the first exposure to opiates and stems from opiate activation of
N-methyl-
d-aspartate-dependent pain facilitatory systems.</description><identifier>ISSN: 0306-4522</identifier><identifier>EISSN: 1873-7544</identifier><identifier>DOI: 10.1016/S0306-4522(97)00556-3</identifier><identifier>PMID: 9539228</identifier><identifier>CODEN: NRSCDN</identifier><language>eng</language><publisher>Oxford: Elsevier Ltd</publisher><subject>acute tolerance ; analgesia ; Analgesics, Opioid - pharmacology ; Analysis of Variance ; Animals ; Biological and medical sciences ; Dizocilpine Maleate - pharmacology ; Drug Tolerance - physiology ; heroin ; Heroin - pharmacology ; Hyperalgesia - chemically induced ; Hyperalgesia - physiopathology ; Male ; Medical sciences ; Naloxone - pharmacology ; Neuropharmacology ; Neurotransmitters. Neurotransmission. Receptors ; NMDA receptors ; opiates ; Pain - physiopathology ; pain facilitatory systems ; Pain Measurement - methods ; Peptidergic system (neuropeptide, opioid peptide, opiates...). Adenosinergic and purinergic systems ; Pharmacology. Drug treatments ; Rats ; Rats, Sprague-Dawley ; Reaction Time</subject><ispartof>Neuroscience, 1998-05, Vol.84 (2), p.583-589</ispartof><rights>1998 IBRO</rights><rights>1998 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c445t-485b0ec0926769760db1d50fe0b9224711d953badff884ac747063fccdf94a063</citedby><cites>FETCH-LOGICAL-c445t-485b0ec0926769760db1d50fe0b9224711d953badff884ac747063fccdf94a063</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(97)00556-3$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3548,27922,27923,45993</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2166725$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9539228$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Larcher, A</creatorcontrib><creatorcontrib>Laulin, J.P</creatorcontrib><creatorcontrib>Celerier, E</creatorcontrib><creatorcontrib>Le Moal, M</creatorcontrib><creatorcontrib>Simonnet, G</creatorcontrib><title>Acute tolerance associated with a single opiate administration: involvement of N-methyl- d-aspartate-dependent pain facilitatory systems</title><title>Neuroscience</title><addtitle>Neuroscience</addtitle><description>Mechanisms underlying the development of acute tolerance to the analgesic effect of opiates were investigated. In the rat tail-flick test, administration of naloxone (1
mg/kg, s.c.) 40
min after heroin (1
mg/kg, s.c.) was shown to induce hyperalgesia, indicative of a short-onset, opiate-activated pain facilitatory systems masking the opiate analgesia. Pretreatment with the
N-methyl-
d-aspartate receptor antagonist dizocilpine maleate blocked, in a dose-dependent manner, the naloxone-induced hyperalgesia and potentiated the heroin-induced analgesia. Using a schedule of two successive injections of 1
mg/kg heroin, acute tolerance was indicated by a marked reduction (−52%) in analgesia induced by the second dose. After pretreatment with dizocilpine maleate, the acute tolerance was abolished and the analgesic effects of both injections of heroin were strongly potentiated.
These observations indicate that acute tolerance appears after the first exposure to opiates and stems from opiate activation of
N-methyl-
d-aspartate-dependent pain facilitatory systems.</description><subject>acute tolerance</subject><subject>analgesia</subject><subject>Analgesics, Opioid - pharmacology</subject><subject>Analysis of Variance</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Dizocilpine Maleate - pharmacology</subject><subject>Drug Tolerance - physiology</subject><subject>heroin</subject><subject>Heroin - pharmacology</subject><subject>Hyperalgesia - chemically induced</subject><subject>Hyperalgesia - physiopathology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Naloxone - pharmacology</subject><subject>Neuropharmacology</subject><subject>Neurotransmitters. Neurotransmission. Receptors</subject><subject>NMDA receptors</subject><subject>opiates</subject><subject>Pain - physiopathology</subject><subject>pain facilitatory systems</subject><subject>Pain Measurement - methods</subject><subject>Peptidergic system (neuropeptide, opioid peptide, opiates...). Adenosinergic and purinergic systems</subject><subject>Pharmacology. Drug treatments</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Reaction Time</subject><issn>0306-4522</issn><issn>1873-7544</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc2OFCEUhYnRjO3oI0zCwhhd4EAVP1VuzGQy_iQTXahrQsHFwVQVJdA96TeYx5aa7vRWNhDOdy_ccxC6YPQ9o0xe_qAtlYSLpnnbq3eUCiFJ-wRtWKdaogTnT9HmhDxHL3L-Q-sSvD1DZ71o-6bpNujhym4L4BJHSGa2gE3O0QZTwOH7UO6wwTnMv0fAcVlvsXFTmEMuyZQQ5w84zLs47mCCueDo8TcyQbnbjwQ7YvJiUqlFxMECs1uRxYQZe2PDGKoS0x7nfS4w5ZfomTdjhlfH_Rz9-nTz8_oLuf3--ev11S2xnItCeCcGCpb2jVSyV5K6gTlBPdChDsQVY67ONhjnfddxYxVXVLbeWud7burxHL059F1S_LuFXPQUsoVxNDPEbdZMVmuo6isoDqBNMecEXi8pTCbtNaN6TUA_JqBXe3Wv9GMCuq11F8cHtsME7lR1tLzqr4-6ydaMfrU95BPWMClVIyr28YBBNWMXIOlsA9SEXEhgi3Yx_Ocj_wCcgaUz</recordid><startdate>19980501</startdate><enddate>19980501</enddate><creator>Larcher, A</creator><creator>Laulin, J.P</creator><creator>Celerier, E</creator><creator>Le Moal, M</creator><creator>Simonnet, G</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>7TK</scope></search><sort><creationdate>19980501</creationdate><title>Acute tolerance associated with a single opiate administration: involvement of N-methyl- d-aspartate-dependent pain facilitatory systems</title><author>Larcher, A ; Laulin, J.P ; Celerier, E ; Le Moal, M ; Simonnet, G</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c445t-485b0ec0926769760db1d50fe0b9224711d953badff884ac747063fccdf94a063</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>acute tolerance</topic><topic>analgesia</topic><topic>Analgesics, Opioid - pharmacology</topic><topic>Analysis of Variance</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Dizocilpine Maleate - pharmacology</topic><topic>Drug Tolerance - physiology</topic><topic>heroin</topic><topic>Heroin - pharmacology</topic><topic>Hyperalgesia - chemically induced</topic><topic>Hyperalgesia - physiopathology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Naloxone - pharmacology</topic><topic>Neuropharmacology</topic><topic>Neurotransmitters. Neurotransmission. Receptors</topic><topic>NMDA receptors</topic><topic>opiates</topic><topic>Pain - physiopathology</topic><topic>pain facilitatory systems</topic><topic>Pain Measurement - methods</topic><topic>Peptidergic system (neuropeptide, opioid peptide, opiates...). Adenosinergic and purinergic systems</topic><topic>Pharmacology. Drug treatments</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Reaction Time</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Larcher, A</creatorcontrib><creatorcontrib>Laulin, J.P</creatorcontrib><creatorcontrib>Celerier, E</creatorcontrib><creatorcontrib>Le Moal, M</creatorcontrib><creatorcontrib>Simonnet, G</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>Neurosciences Abstracts</collection><jtitle>Neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Larcher, A</au><au>Laulin, J.P</au><au>Celerier, E</au><au>Le Moal, M</au><au>Simonnet, G</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Acute tolerance associated with a single opiate administration: involvement of N-methyl- d-aspartate-dependent pain facilitatory systems</atitle><jtitle>Neuroscience</jtitle><addtitle>Neuroscience</addtitle><date>1998-05-01</date><risdate>1998</risdate><volume>84</volume><issue>2</issue><spage>583</spage><epage>589</epage><pages>583-589</pages><issn>0306-4522</issn><eissn>1873-7544</eissn><coden>NRSCDN</coden><abstract>Mechanisms underlying the development of acute tolerance to the analgesic effect of opiates were investigated. In the rat tail-flick test, administration of naloxone (1
mg/kg, s.c.) 40
min after heroin (1
mg/kg, s.c.) was shown to induce hyperalgesia, indicative of a short-onset, opiate-activated pain facilitatory systems masking the opiate analgesia. Pretreatment with the
N-methyl-
d-aspartate receptor antagonist dizocilpine maleate blocked, in a dose-dependent manner, the naloxone-induced hyperalgesia and potentiated the heroin-induced analgesia. Using a schedule of two successive injections of 1
mg/kg heroin, acute tolerance was indicated by a marked reduction (−52%) in analgesia induced by the second dose. After pretreatment with dizocilpine maleate, the acute tolerance was abolished and the analgesic effects of both injections of heroin were strongly potentiated.
These observations indicate that acute tolerance appears after the first exposure to opiates and stems from opiate activation of
N-methyl-
d-aspartate-dependent pain facilitatory systems.</abstract><cop>Oxford</cop><pub>Elsevier Ltd</pub><pmid>9539228</pmid><doi>10.1016/S0306-4522(97)00556-3</doi><tpages>7</tpages></addata></record> |
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| subjects | acute tolerance analgesia Analgesics, Opioid - pharmacology Analysis of Variance Animals Biological and medical sciences Dizocilpine Maleate - pharmacology Drug Tolerance - physiology heroin Heroin - pharmacology Hyperalgesia - chemically induced Hyperalgesia - physiopathology Male Medical sciences Naloxone - pharmacology Neuropharmacology Neurotransmitters. Neurotransmission. Receptors NMDA receptors opiates Pain - physiopathology pain facilitatory systems Pain Measurement - methods Peptidergic system (neuropeptide, opioid peptide, opiates...). Adenosinergic and purinergic systems Pharmacology. Drug treatments Rats Rats, Sprague-Dawley Reaction Time |
| title | Acute tolerance associated with a single opiate administration: involvement of N-methyl- d-aspartate-dependent pain facilitatory systems |
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