Noradrenergic-serotonergic interactions and nociception in the rat
Spinal noradrenaline (NA) depletion in rats, via either systemic N-2-chloroethyl-N-ethyl-2-bromobenzylamine (DSP4) or intrathecal 6-hydroxydopamine (6-OHDA), reversed and/or abolished the analgesic effects of the 5-hydroxytryptamine (5-HT) agonists, 5-methoxy-N,N-dimethyltryptamine (5-MeODMT) and p-...
Gespeichert in:
| Veröffentlicht in: | European journal of pharmacology 1986-01, Vol.120 (3), p.295-307 |
|---|---|
| Hauptverfasser: | , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 307 |
|---|---|
| container_issue | 3 |
| container_start_page | 295 |
| container_title | European journal of pharmacology |
| container_volume | 120 |
| creator | Archer, Trevor Jonsson, Gösta Minor, Bruce G. Post, Claes |
| description | Spinal noradrenaline (NA) depletion in rats, via either systemic N-2-chloroethyl-N-ethyl-2-bromobenzylamine (DSP4) or intrathecal 6-hydroxydopamine (6-OHDA), reversed and/or abolished the analgesic effects of the 5-hydroxytryptamine (5-HT) agonists, 5-methoxy-N,N-dimethyltryptamine (5-MeODMT) and p-chloroamphetamine (PCA), in shock titration, hot-plate and tail-flick measures of pain sensitivity. Spinal NA depletion also abolished the analgesic effects of 5-HT itself, administered intrathecally, in all three nociception tests and potentiated the analgesic effects of intrathecal NA, a demonstration of receptor supersensitivity. Spinal 5-HT depletion, via intrathecal 5,7-dihydroxytryptamine (5,7-DHT), only attenuated 5-MeODMT-induced analgesia in the tail-flick test but potentiated the 5-MeODMT effect in the hot-plate test. Intrathecal 5,7-DHT treatment caused a drastic potentiation of NA-induced analgesia in the shock titration and tail-flick tests but not in the hot-plate test. Biochemical analyses confirmed the NA and 5-HT depletion. The spinal noradrenergic system appears to be an important tonic factor modulating the function of the descending 5-hydroxytryptaminergic pathway. |
| doi_str_mv | 10.1016/0014-2999(86)90470-X |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_76709998</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>001429998690470X</els_id><sourcerecordid>76709998</sourcerecordid><originalsourceid>FETCH-LOGICAL-c508t-da52bb0c17c9fa15d4e3aec063e812f6a4394228e811b882cd8766369d5157b83</originalsourceid><addsrcrecordid>eNqFkE1LxDAQhoMo67r6DxR6ENFDNUmbr4ugi1-w6EXBW0iTqUa6zZp0Bf-9XbvsUU_DzPvMkDwIHRJ8TjDhFxiTMqdKqVPJzxQuBc5ft9CYSKFyLAjdRuMNsov2UvrAGDNF2QiNCixJweQYXT-GaFyEFuKbt3mCGLowNJlvO4jGdj60KTOty9pgvYXFatCHWfcOWTTdPtqpTZPgYF0n6OX25nl6n8-e7h6mV7PcMiy73BlGqwpbIqyqDWGuhMKAxbwASWjNTVmoklLZd6SSklonBecFV44RJipZTNDJcHcRw-cSUqfnPlloGtNCWCYtuMD9V_8HSclZyajqwXIAbQwpRaj1Ivq5id-aYL1yrFcC9Uqgllz_Otav_drR-v6ymoPbLK2l9vnxOjfJmqaOprU-bTApWCGJ6LHLAYNe2peHqJP10FpwPoLttAv-73f8AC2Gl6s</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>14654529</pqid></control><display><type>article</type><title>Noradrenergic-serotonergic interactions and nociception in the rat</title><source>MEDLINE</source><source>Elsevier ScienceDirect Journals</source><creator>Archer, Trevor ; Jonsson, Gösta ; Minor, Bruce G. ; Post, Claes</creator><creatorcontrib>Archer, Trevor ; Jonsson, Gösta ; Minor, Bruce G. ; Post, Claes</creatorcontrib><description>Spinal noradrenaline (NA) depletion in rats, via either systemic N-2-chloroethyl-N-ethyl-2-bromobenzylamine (DSP4) or intrathecal 6-hydroxydopamine (6-OHDA), reversed and/or abolished the analgesic effects of the 5-hydroxytryptamine (5-HT) agonists, 5-methoxy-N,N-dimethyltryptamine (5-MeODMT) and p-chloroamphetamine (PCA), in shock titration, hot-plate and tail-flick measures of pain sensitivity. Spinal NA depletion also abolished the analgesic effects of 5-HT itself, administered intrathecally, in all three nociception tests and potentiated the analgesic effects of intrathecal NA, a demonstration of receptor supersensitivity. Spinal 5-HT depletion, via intrathecal 5,7-dihydroxytryptamine (5,7-DHT), only attenuated 5-MeODMT-induced analgesia in the tail-flick test but potentiated the 5-MeODMT effect in the hot-plate test. Intrathecal 5,7-DHT treatment caused a drastic potentiation of NA-induced analgesia in the shock titration and tail-flick tests but not in the hot-plate test. Biochemical analyses confirmed the NA and 5-HT depletion. The spinal noradrenergic system appears to be an important tonic factor modulating the function of the descending 5-hydroxytryptaminergic pathway.</description><identifier>ISSN: 0014-2999</identifier><identifier>EISSN: 1879-0712</identifier><identifier>DOI: 10.1016/0014-2999(86)90470-X</identifier><identifier>PMID: 3081358</identifier><identifier>CODEN: EJPHAZ</identifier><language>eng</language><publisher>Amsterdam: Elsevier B.V</publisher><subject>5,7-Dihydroxytryptamine - pharmacology ; Analgesia ; Animals ; Benzylamines - pharmacology ; Biological and medical sciences ; Blockade ; Catecholaminergic system ; Hydroxydopamines - pharmacology ; Male ; Medical sciences ; Methoxydimethyltryptamines - pharmacology ; Neuropharmacology ; Neurotransmitters. Neurotransmission. Receptors ; Nociceptors - physiology ; Noradrenaline ; Norepinephrine - physiology ; Oxidopamine ; Pharmacology. Drug treatments ; Potentiation ; Rats ; Rats, Inbred Strains ; Reaction Time - drug effects ; Reversal ; Serotonin ; Serotonin - physiology ; Spinal cord</subject><ispartof>European journal of pharmacology, 1986-01, Vol.120 (3), p.295-307</ispartof><rights>1986</rights><rights>1986 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c508t-da52bb0c17c9fa15d4e3aec063e812f6a4394228e811b882cd8766369d5157b83</citedby><cites>FETCH-LOGICAL-c508t-da52bb0c17c9fa15d4e3aec063e812f6a4394228e811b882cd8766369d5157b83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/0014-2999(86)90470-X$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3536,27903,27904,45974</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=8753817$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/3081358$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Archer, Trevor</creatorcontrib><creatorcontrib>Jonsson, Gösta</creatorcontrib><creatorcontrib>Minor, Bruce G.</creatorcontrib><creatorcontrib>Post, Claes</creatorcontrib><title>Noradrenergic-serotonergic interactions and nociception in the rat</title><title>European journal of pharmacology</title><addtitle>Eur J Pharmacol</addtitle><description>Spinal noradrenaline (NA) depletion in rats, via either systemic N-2-chloroethyl-N-ethyl-2-bromobenzylamine (DSP4) or intrathecal 6-hydroxydopamine (6-OHDA), reversed and/or abolished the analgesic effects of the 5-hydroxytryptamine (5-HT) agonists, 5-methoxy-N,N-dimethyltryptamine (5-MeODMT) and p-chloroamphetamine (PCA), in shock titration, hot-plate and tail-flick measures of pain sensitivity. Spinal NA depletion also abolished the analgesic effects of 5-HT itself, administered intrathecally, in all three nociception tests and potentiated the analgesic effects of intrathecal NA, a demonstration of receptor supersensitivity. Spinal 5-HT depletion, via intrathecal 5,7-dihydroxytryptamine (5,7-DHT), only attenuated 5-MeODMT-induced analgesia in the tail-flick test but potentiated the 5-MeODMT effect in the hot-plate test. Intrathecal 5,7-DHT treatment caused a drastic potentiation of NA-induced analgesia in the shock titration and tail-flick tests but not in the hot-plate test. Biochemical analyses confirmed the NA and 5-HT depletion. The spinal noradrenergic system appears to be an important tonic factor modulating the function of the descending 5-hydroxytryptaminergic pathway.</description><subject>5,7-Dihydroxytryptamine - pharmacology</subject><subject>Analgesia</subject><subject>Animals</subject><subject>Benzylamines - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Blockade</subject><subject>Catecholaminergic system</subject><subject>Hydroxydopamines - pharmacology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Methoxydimethyltryptamines - pharmacology</subject><subject>Neuropharmacology</subject><subject>Neurotransmitters. Neurotransmission. Receptors</subject><subject>Nociceptors - physiology</subject><subject>Noradrenaline</subject><subject>Norepinephrine - physiology</subject><subject>Oxidopamine</subject><subject>Pharmacology. Drug treatments</subject><subject>Potentiation</subject><subject>Rats</subject><subject>Rats, Inbred Strains</subject><subject>Reaction Time - drug effects</subject><subject>Reversal</subject><subject>Serotonin</subject><subject>Serotonin - physiology</subject><subject>Spinal cord</subject><issn>0014-2999</issn><issn>1879-0712</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1986</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkE1LxDAQhoMo67r6DxR6ENFDNUmbr4ugi1-w6EXBW0iTqUa6zZp0Bf-9XbvsUU_DzPvMkDwIHRJ8TjDhFxiTMqdKqVPJzxQuBc5ft9CYSKFyLAjdRuMNsov2UvrAGDNF2QiNCixJweQYXT-GaFyEFuKbt3mCGLowNJlvO4jGdj60KTOty9pgvYXFatCHWfcOWTTdPtqpTZPgYF0n6OX25nl6n8-e7h6mV7PcMiy73BlGqwpbIqyqDWGuhMKAxbwASWjNTVmoklLZd6SSklonBecFV44RJipZTNDJcHcRw-cSUqfnPlloGtNCWCYtuMD9V_8HSclZyajqwXIAbQwpRaj1Ivq5id-aYL1yrFcC9Uqgllz_Otav_drR-v6ymoPbLK2l9vnxOjfJmqaOprU-bTApWCGJ6LHLAYNe2peHqJP10FpwPoLttAv-73f8AC2Gl6s</recordid><startdate>19860129</startdate><enddate>19860129</enddate><creator>Archer, Trevor</creator><creator>Jonsson, Gösta</creator><creator>Minor, Bruce G.</creator><creator>Post, Claes</creator><general>Elsevier B.V</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><scope>7X8</scope></search><sort><creationdate>19860129</creationdate><title>Noradrenergic-serotonergic interactions and nociception in the rat</title><author>Archer, Trevor ; Jonsson, Gösta ; Minor, Bruce G. ; Post, Claes</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c508t-da52bb0c17c9fa15d4e3aec063e812f6a4394228e811b882cd8766369d5157b83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1986</creationdate><topic>5,7-Dihydroxytryptamine - pharmacology</topic><topic>Analgesia</topic><topic>Animals</topic><topic>Benzylamines - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Blockade</topic><topic>Catecholaminergic system</topic><topic>Hydroxydopamines - pharmacology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Methoxydimethyltryptamines - pharmacology</topic><topic>Neuropharmacology</topic><topic>Neurotransmitters. Neurotransmission. Receptors</topic><topic>Nociceptors - physiology</topic><topic>Noradrenaline</topic><topic>Norepinephrine - physiology</topic><topic>Oxidopamine</topic><topic>Pharmacology. Drug treatments</topic><topic>Potentiation</topic><topic>Rats</topic><topic>Rats, Inbred Strains</topic><topic>Reaction Time - drug effects</topic><topic>Reversal</topic><topic>Serotonin</topic><topic>Serotonin - physiology</topic><topic>Spinal cord</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Archer, Trevor</creatorcontrib><creatorcontrib>Jonsson, Gösta</creatorcontrib><creatorcontrib>Minor, Bruce G.</creatorcontrib><creatorcontrib>Post, Claes</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><collection>MEDLINE - Academic</collection><jtitle>European journal of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Archer, Trevor</au><au>Jonsson, Gösta</au><au>Minor, Bruce G.</au><au>Post, Claes</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Noradrenergic-serotonergic interactions and nociception in the rat</atitle><jtitle>European journal of pharmacology</jtitle><addtitle>Eur J Pharmacol</addtitle><date>1986-01-29</date><risdate>1986</risdate><volume>120</volume><issue>3</issue><spage>295</spage><epage>307</epage><pages>295-307</pages><issn>0014-2999</issn><eissn>1879-0712</eissn><coden>EJPHAZ</coden><abstract>Spinal noradrenaline (NA) depletion in rats, via either systemic N-2-chloroethyl-N-ethyl-2-bromobenzylamine (DSP4) or intrathecal 6-hydroxydopamine (6-OHDA), reversed and/or abolished the analgesic effects of the 5-hydroxytryptamine (5-HT) agonists, 5-methoxy-N,N-dimethyltryptamine (5-MeODMT) and p-chloroamphetamine (PCA), in shock titration, hot-plate and tail-flick measures of pain sensitivity. Spinal NA depletion also abolished the analgesic effects of 5-HT itself, administered intrathecally, in all three nociception tests and potentiated the analgesic effects of intrathecal NA, a demonstration of receptor supersensitivity. Spinal 5-HT depletion, via intrathecal 5,7-dihydroxytryptamine (5,7-DHT), only attenuated 5-MeODMT-induced analgesia in the tail-flick test but potentiated the 5-MeODMT effect in the hot-plate test. Intrathecal 5,7-DHT treatment caused a drastic potentiation of NA-induced analgesia in the shock titration and tail-flick tests but not in the hot-plate test. Biochemical analyses confirmed the NA and 5-HT depletion. The spinal noradrenergic system appears to be an important tonic factor modulating the function of the descending 5-hydroxytryptaminergic pathway.</abstract><cop>Amsterdam</cop><pub>Elsevier B.V</pub><pmid>3081358</pmid><doi>10.1016/0014-2999(86)90470-X</doi><tpages>13</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0014-2999 |
| ispartof | European journal of pharmacology, 1986-01, Vol.120 (3), p.295-307 |
| issn | 0014-2999 1879-0712 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_76709998 |
| source | MEDLINE; Elsevier ScienceDirect Journals |
| subjects | 5,7-Dihydroxytryptamine - pharmacology Analgesia Animals Benzylamines - pharmacology Biological and medical sciences Blockade Catecholaminergic system Hydroxydopamines - pharmacology Male Medical sciences Methoxydimethyltryptamines - pharmacology Neuropharmacology Neurotransmitters. Neurotransmission. Receptors Nociceptors - physiology Noradrenaline Norepinephrine - physiology Oxidopamine Pharmacology. Drug treatments Potentiation Rats Rats, Inbred Strains Reaction Time - drug effects Reversal Serotonin Serotonin - physiology Spinal cord |
| title | Noradrenergic-serotonergic interactions and nociception in the rat |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-22T06%3A29%3A13IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Noradrenergic-serotonergic%20interactions%20and%20nociception%20in%20the%20rat&rft.jtitle=European%20journal%20of%20pharmacology&rft.au=Archer,%20Trevor&rft.date=1986-01-29&rft.volume=120&rft.issue=3&rft.spage=295&rft.epage=307&rft.pages=295-307&rft.issn=0014-2999&rft.eissn=1879-0712&rft.coden=EJPHAZ&rft_id=info:doi/10.1016/0014-2999(86)90470-X&rft_dat=%3Cproquest_cross%3E76709998%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=14654529&rft_id=info:pmid/3081358&rft_els_id=001429998690470X&rfr_iscdi=true |