Re-evaluation of lisuride pharmacology: 5-hydroxytryptamine1A receptor-mediated behavioral effects overlap its other properties in rats
There is substantial evidence that lisuride can produce effects linked to 5-HT(1A) receptor occupancy. Nevertheless, this action has generally been ignored in the mechanism of action of lisuride, in favor of an exclusive role for dopamine receptors in considering its antiparkinsonian effects, or an...
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| Veröffentlicht in: | Psychopharmacologia 2002-10, Vol.164 (1), p.93-107 |
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| creator | MARONA-LEWICKA, Danuta KURRASCH-ORBAUGH, Deborah M SELKEN, Jennifer R CUMBAY, Medhane G LISNICCHIA, Joshua G NICHOLS, David E |
| description | There is substantial evidence that lisuride can produce effects linked to 5-HT(1A) receptor occupancy. Nevertheless, this action has generally been ignored in the mechanism of action of lisuride, in favor of an exclusive role for dopamine receptors in considering its antiparkinsonian effects, or an exclusive role of 5-HT(2A/2C) receptor activation in hallucinogenesis. These conclusions are surprising when one considers that the potent interaction of lisuride with 5-HT(1A) receptors has been demonstrated in several different laboratories and that activation of 5-HT(1A) and 5-HT(1B) receptors can modulate dopaminergically mediated responses.
The lack of full substitution of lisuride for lysergic acid diethylamide (LSD) in drug discrimination experiments and induction of a pronounced 5-HT syndrome by this compound at relatively low doses convinced us to execute two series of experiments that might explain the primary mechanism responsible for lisuride-mediated biological effects and its paradoxical classification as a dopamine agonist in the literature.
In drug discrimination studies, lisuride fully mimicked the 5-HT(1A) agonist LY 293284, only partially substituted for LSD and DOI, and failed to substitute for (+)-amphetamine. Lisuride produced a significant dose-related increase in flat body posture, forepaw treading, and lower-lip retraction which reflect a modulation of behavior by action at central 5-HT(1A) receptors. Only pMPPI [4-iodo-N-[2-[4-(methoxyphenyl)-1-piperazinyl]ethyl]-N-2-pyridynyl-benzamide hydrochloride], a selective 5-HT(1A) antagonist, was effective in inhibiting all 5-HT syndrome behaviors produced by lisuride, whereas pMPPI was without effect on any behavior induced by LSD. Lisuride dose dependently decreased body temperature in rats with a potency similar to that of the selective 5-HT(1A) agonist LY 293284. The hypothermic effect of lisuride was prevented by pre-injection of pMPPI, but not by ketanserin or haloperidol.
We have demonstrated that the behavioral effects of low doses of lisuride are clearly mediated by stimulation of 5-HT(1A) receptors. |
| doi_str_mv | 10.1007/s00213-002-1141-z |
| format | Article |
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The lack of full substitution of lisuride for lysergic acid diethylamide (LSD) in drug discrimination experiments and induction of a pronounced 5-HT syndrome by this compound at relatively low doses convinced us to execute two series of experiments that might explain the primary mechanism responsible for lisuride-mediated biological effects and its paradoxical classification as a dopamine agonist in the literature.
In drug discrimination studies, lisuride fully mimicked the 5-HT(1A) agonist LY 293284, only partially substituted for LSD and DOI, and failed to substitute for (+)-amphetamine. Lisuride produced a significant dose-related increase in flat body posture, forepaw treading, and lower-lip retraction which reflect a modulation of behavior by action at central 5-HT(1A) receptors. Only pMPPI [4-iodo-N-[2-[4-(methoxyphenyl)-1-piperazinyl]ethyl]-N-2-pyridynyl-benzamide hydrochloride], a selective 5-HT(1A) antagonist, was effective in inhibiting all 5-HT syndrome behaviors produced by lisuride, whereas pMPPI was without effect on any behavior induced by LSD. Lisuride dose dependently decreased body temperature in rats with a potency similar to that of the selective 5-HT(1A) agonist LY 293284. The hypothermic effect of lisuride was prevented by pre-injection of pMPPI, but not by ketanserin or haloperidol.
We have demonstrated that the behavioral effects of low doses of lisuride are clearly mediated by stimulation of 5-HT(1A) receptors.</description><identifier>ISSN: 0033-3158</identifier><identifier>EISSN: 1432-2072</identifier><identifier>DOI: 10.1007/s00213-002-1141-z</identifier><identifier>PMID: 12373423</identifier><identifier>CODEN: PSYPAG</identifier><language>eng</language><publisher>Berlin: Springer</publisher><subject>Animals ; Anticonvulsants. Antiepileptics. Antiparkinson agents ; Biological and medical sciences ; Body Temperature - drug effects ; Body Temperature - physiology ; CHO Cells ; Cricetinae ; Discrimination (Psychology) - drug effects ; Discrimination (Psychology) - physiology ; Dose-Response Relationship, Drug ; Humans ; Lisuride - metabolism ; Lisuride - pharmacology ; Lysergic Acid Diethylamide - metabolism ; Lysergic Acid Diethylamide - pharmacology ; Male ; Medical sciences ; Neuropharmacology ; Pharmacology. Drug treatments ; Rats ; Rats, Sprague-Dawley ; Receptors, Serotonin - metabolism ; Receptors, Serotonin - physiology ; Receptors, Serotonin, 5-HT1 ; Serotonin Receptor Agonists - metabolism ; Serotonin Receptor Agonists - pharmacology</subject><ispartof>Psychopharmacologia, 2002-10, Vol.164 (1), p.93-107</ispartof><rights>2003 INIST-CNRS</rights><rights>Copyright Springer-Verlag 2002</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781,27905,27906</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=13974661$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12373423$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>MARONA-LEWICKA, Danuta</creatorcontrib><creatorcontrib>KURRASCH-ORBAUGH, Deborah M</creatorcontrib><creatorcontrib>SELKEN, Jennifer R</creatorcontrib><creatorcontrib>CUMBAY, Medhane G</creatorcontrib><creatorcontrib>LISNICCHIA, Joshua G</creatorcontrib><creatorcontrib>NICHOLS, David E</creatorcontrib><title>Re-evaluation of lisuride pharmacology: 5-hydroxytryptamine1A receptor-mediated behavioral effects overlap its other properties in rats</title><title>Psychopharmacologia</title><addtitle>Psychopharmacology (Berl)</addtitle><description>There is substantial evidence that lisuride can produce effects linked to 5-HT(1A) receptor occupancy. Nevertheless, this action has generally been ignored in the mechanism of action of lisuride, in favor of an exclusive role for dopamine receptors in considering its antiparkinsonian effects, or an exclusive role of 5-HT(2A/2C) receptor activation in hallucinogenesis. These conclusions are surprising when one considers that the potent interaction of lisuride with 5-HT(1A) receptors has been demonstrated in several different laboratories and that activation of 5-HT(1A) and 5-HT(1B) receptors can modulate dopaminergically mediated responses.
The lack of full substitution of lisuride for lysergic acid diethylamide (LSD) in drug discrimination experiments and induction of a pronounced 5-HT syndrome by this compound at relatively low doses convinced us to execute two series of experiments that might explain the primary mechanism responsible for lisuride-mediated biological effects and its paradoxical classification as a dopamine agonist in the literature.
In drug discrimination studies, lisuride fully mimicked the 5-HT(1A) agonist LY 293284, only partially substituted for LSD and DOI, and failed to substitute for (+)-amphetamine. Lisuride produced a significant dose-related increase in flat body posture, forepaw treading, and lower-lip retraction which reflect a modulation of behavior by action at central 5-HT(1A) receptors. Only pMPPI [4-iodo-N-[2-[4-(methoxyphenyl)-1-piperazinyl]ethyl]-N-2-pyridynyl-benzamide hydrochloride], a selective 5-HT(1A) antagonist, was effective in inhibiting all 5-HT syndrome behaviors produced by lisuride, whereas pMPPI was without effect on any behavior induced by LSD. Lisuride dose dependently decreased body temperature in rats with a potency similar to that of the selective 5-HT(1A) agonist LY 293284. The hypothermic effect of lisuride was prevented by pre-injection of pMPPI, but not by ketanserin or haloperidol.
We have demonstrated that the behavioral effects of low doses of lisuride are clearly mediated by stimulation of 5-HT(1A) receptors.</description><subject>Animals</subject><subject>Anticonvulsants. Antiepileptics. Antiparkinson agents</subject><subject>Biological and medical sciences</subject><subject>Body Temperature - drug effects</subject><subject>Body Temperature - physiology</subject><subject>CHO Cells</subject><subject>Cricetinae</subject><subject>Discrimination (Psychology) - drug effects</subject><subject>Discrimination (Psychology) - physiology</subject><subject>Dose-Response Relationship, Drug</subject><subject>Humans</subject><subject>Lisuride - metabolism</subject><subject>Lisuride - pharmacology</subject><subject>Lysergic Acid Diethylamide - metabolism</subject><subject>Lysergic Acid Diethylamide - pharmacology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Neuropharmacology</subject><subject>Pharmacology. Drug treatments</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptors, Serotonin - metabolism</subject><subject>Receptors, Serotonin - physiology</subject><subject>Receptors, Serotonin, 5-HT1</subject><subject>Serotonin Receptor Agonists - metabolism</subject><subject>Serotonin Receptor Agonists - pharmacology</subject><issn>0033-3158</issn><issn>1432-2072</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNpdkE2LFDEQhoMo7rj6A7xIEPQWTSXpSbe3ZfELFgTRc1OTrjhZujttkh5s_4B_2yyOCNah6j08FC8PY09BvgIp7esspQIt6hYABsTPe2wHRiuhpFX32U5KrYWGpr1gj3K-lXVMax6yC1DaaqP0jv36TIJOOK5YQpx59HwMeU1hIL4cMU3o4hi_bW94I47bkOKPraRtKTiFmeCKJ3K0lJjEREPAQgM_0BFPISYcOXlPrmQeT5RGXHi4y-VIiS8pLpRKoMzDzBOW_Jg98DhmenK-l-zru7dfrj-Im0_vP15f3YgFbFdE66A5NNrYrsG9N7Yx2jdeIw2STNvRgYCGweFe2864ofOoqDO-2mkAFJG-ZC___K0Vvq-USz-F7Ggccaa45t6qqqsFWcHn_4G3cU1z7dYraDsjtbqDnp2h9VAN9EsKE6at_-u3Ai_OAGaHo084u5D_cbqzZr8H_RvHQoz0</recordid><startdate>200210</startdate><enddate>200210</enddate><creator>MARONA-LEWICKA, Danuta</creator><creator>KURRASCH-ORBAUGH, Deborah M</creator><creator>SELKEN, Jennifer R</creator><creator>CUMBAY, Medhane G</creator><creator>LISNICCHIA, Joshua G</creator><creator>NICHOLS, David E</creator><general>Springer</general><general>Springer Nature B.V</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>3V.</scope><scope>7QG</scope><scope>7QR</scope><scope>7RV</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>8AO</scope><scope>8FD</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>NAPCQ</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>200210</creationdate><title>Re-evaluation of lisuride pharmacology: 5-hydroxytryptamine1A receptor-mediated behavioral effects overlap its other properties in rats</title><author>MARONA-LEWICKA, Danuta ; KURRASCH-ORBAUGH, Deborah M ; SELKEN, Jennifer R ; CUMBAY, Medhane G ; LISNICCHIA, Joshua G ; NICHOLS, David E</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p179t-8c15b534795a6f47543f5f3aed0e489ebe1eddca63794cd9fa2e94f1145112ee3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Animals</topic><topic>Anticonvulsants. Antiepileptics. Antiparkinson agents</topic><topic>Biological and medical sciences</topic><topic>Body Temperature - drug effects</topic><topic>Body Temperature - physiology</topic><topic>CHO Cells</topic><topic>Cricetinae</topic><topic>Discrimination (Psychology) - drug effects</topic><topic>Discrimination (Psychology) - physiology</topic><topic>Dose-Response Relationship, Drug</topic><topic>Humans</topic><topic>Lisuride - metabolism</topic><topic>Lisuride - pharmacology</topic><topic>Lysergic Acid Diethylamide - metabolism</topic><topic>Lysergic Acid Diethylamide - pharmacology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Neuropharmacology</topic><topic>Pharmacology. Drug treatments</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptors, Serotonin - metabolism</topic><topic>Receptors, Serotonin - physiology</topic><topic>Receptors, Serotonin, 5-HT1</topic><topic>Serotonin Receptor Agonists - metabolism</topic><topic>Serotonin Receptor Agonists - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>MARONA-LEWICKA, Danuta</creatorcontrib><creatorcontrib>KURRASCH-ORBAUGH, Deborah M</creatorcontrib><creatorcontrib>SELKEN, Jennifer R</creatorcontrib><creatorcontrib>CUMBAY, Medhane G</creatorcontrib><creatorcontrib>LISNICCHIA, Joshua G</creatorcontrib><creatorcontrib>NICHOLS, David E</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>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Nursing & Allied Health Database (ProQuest)</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medicine (ProQuest)</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>Psychology Database (ProQuest)</collection><collection>Nursing & Allied Health Premium</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>Psychopharmacologia</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>MARONA-LEWICKA, Danuta</au><au>KURRASCH-ORBAUGH, Deborah M</au><au>SELKEN, Jennifer R</au><au>CUMBAY, Medhane G</au><au>LISNICCHIA, Joshua G</au><au>NICHOLS, David E</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Re-evaluation of lisuride pharmacology: 5-hydroxytryptamine1A receptor-mediated behavioral effects overlap its other properties in rats</atitle><jtitle>Psychopharmacologia</jtitle><addtitle>Psychopharmacology (Berl)</addtitle><date>2002-10</date><risdate>2002</risdate><volume>164</volume><issue>1</issue><spage>93</spage><epage>107</epage><pages>93-107</pages><issn>0033-3158</issn><eissn>1432-2072</eissn><coden>PSYPAG</coden><abstract>There is substantial evidence that lisuride can produce effects linked to 5-HT(1A) receptor occupancy. Nevertheless, this action has generally been ignored in the mechanism of action of lisuride, in favor of an exclusive role for dopamine receptors in considering its antiparkinsonian effects, or an exclusive role of 5-HT(2A/2C) receptor activation in hallucinogenesis. These conclusions are surprising when one considers that the potent interaction of lisuride with 5-HT(1A) receptors has been demonstrated in several different laboratories and that activation of 5-HT(1A) and 5-HT(1B) receptors can modulate dopaminergically mediated responses.
The lack of full substitution of lisuride for lysergic acid diethylamide (LSD) in drug discrimination experiments and induction of a pronounced 5-HT syndrome by this compound at relatively low doses convinced us to execute two series of experiments that might explain the primary mechanism responsible for lisuride-mediated biological effects and its paradoxical classification as a dopamine agonist in the literature.
In drug discrimination studies, lisuride fully mimicked the 5-HT(1A) agonist LY 293284, only partially substituted for LSD and DOI, and failed to substitute for (+)-amphetamine. Lisuride produced a significant dose-related increase in flat body posture, forepaw treading, and lower-lip retraction which reflect a modulation of behavior by action at central 5-HT(1A) receptors. Only pMPPI [4-iodo-N-[2-[4-(methoxyphenyl)-1-piperazinyl]ethyl]-N-2-pyridynyl-benzamide hydrochloride], a selective 5-HT(1A) antagonist, was effective in inhibiting all 5-HT syndrome behaviors produced by lisuride, whereas pMPPI was without effect on any behavior induced by LSD. Lisuride dose dependently decreased body temperature in rats with a potency similar to that of the selective 5-HT(1A) agonist LY 293284. The hypothermic effect of lisuride was prevented by pre-injection of pMPPI, but not by ketanserin or haloperidol.
We have demonstrated that the behavioral effects of low doses of lisuride are clearly mediated by stimulation of 5-HT(1A) receptors.</abstract><cop>Berlin</cop><pub>Springer</pub><pmid>12373423</pmid><doi>10.1007/s00213-002-1141-z</doi><tpages>15</tpages></addata></record> |
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| subjects | Animals Anticonvulsants. Antiepileptics. Antiparkinson agents Biological and medical sciences Body Temperature - drug effects Body Temperature - physiology CHO Cells Cricetinae Discrimination (Psychology) - drug effects Discrimination (Psychology) - physiology Dose-Response Relationship, Drug Humans Lisuride - metabolism Lisuride - pharmacology Lysergic Acid Diethylamide - metabolism Lysergic Acid Diethylamide - pharmacology Male Medical sciences Neuropharmacology Pharmacology. Drug treatments Rats Rats, Sprague-Dawley Receptors, Serotonin - metabolism Receptors, Serotonin - physiology Receptors, Serotonin, 5-HT1 Serotonin Receptor Agonists - metabolism Serotonin Receptor Agonists - pharmacology |
| title | Re-evaluation of lisuride pharmacology: 5-hydroxytryptamine1A receptor-mediated behavioral effects overlap its other properties in rats |
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