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Ethanol-induced dopamine elevation in the rat — Modulatory effects by subchronic treatment with nicotinic drugs
Chronic nicotine administration is associated with increased ethanol consumption in laboratory animals and in humans. Some smokers report less sedation during acute ethanol intoxication after nicotine administration and the sedative effects from ethanol are mediated by inhibitory GABA A-receptors. I...
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| Published in: | European journal of pharmacology 2007-01, Vol.555 (2), p.139-147 |
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| container_end_page | 147 |
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| container_title | European journal of pharmacology |
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| creator | Löf, Elin Chau, Pei Pei Stomberg, Rosita Söderpalm, Bo |
| description | Chronic nicotine administration is associated with increased ethanol consumption in laboratory animals and in humans. Some smokers report less sedation during acute ethanol intoxication after nicotine administration and the sedative effects from ethanol are mediated by inhibitory GABA
A-receptors. In a series of
in vivo microdialysis experiments we investigated whether subchronic pre-treatment with nicotinic drugs known to enhance ethanol consumption in the rat (nicotine or the peripheral nicotinic antagonist hexamethonium) could modulate the alterations in extracellular dopamine observed in response to administration of ethanol or the sedative GABA
A-agonist diazepam. In the nucleus accumbens and the dorsal striatum, systemic and/or local ethanol administration resulted in transient increases in extracellular dopamine levels that returned to baseline before the local levels of ethanol started to decline. In hexamethonium pre-treated rats, however, the nucleus accumbens dopamine levels were time-locked to the ethanol levels in the same area after systemic or local ethanol administration. Perfusion of diazepam into the nucleus accumbens produced a significant reduction in nucleus accumbens dopamine in controls. Prior subchronic treatment with nicotine or hexamethonium abolished this effect. The present results suggest that subchronic treatment with the nicotinic acetylcholine receptor antagonist hexamethonium reduces a GABA
A-R mediated counteraction of the nucleus accumbens dopamine response to ethanol. Additionally, we demonstrate that modulation of nicotinic receptors may reduce the sensitivity of GABA
A receptors to benzodiazepines. These phenomena may offer a novel explanation to why nicotine and alcohol are often co-abused. |
| doi_str_mv | 10.1016/j.ejphar.2006.10.056 |
| format | article |
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A-receptors. In a series of
in vivo microdialysis experiments we investigated whether subchronic pre-treatment with nicotinic drugs known to enhance ethanol consumption in the rat (nicotine or the peripheral nicotinic antagonist hexamethonium) could modulate the alterations in extracellular dopamine observed in response to administration of ethanol or the sedative GABA
A-agonist diazepam. In the nucleus accumbens and the dorsal striatum, systemic and/or local ethanol administration resulted in transient increases in extracellular dopamine levels that returned to baseline before the local levels of ethanol started to decline. In hexamethonium pre-treated rats, however, the nucleus accumbens dopamine levels were time-locked to the ethanol levels in the same area after systemic or local ethanol administration. Perfusion of diazepam into the nucleus accumbens produced a significant reduction in nucleus accumbens dopamine in controls. Prior subchronic treatment with nicotine or hexamethonium abolished this effect. The present results suggest that subchronic treatment with the nicotinic acetylcholine receptor antagonist hexamethonium reduces a GABA
A-R mediated counteraction of the nucleus accumbens dopamine response to ethanol. Additionally, we demonstrate that modulation of nicotinic receptors may reduce the sensitivity of GABA
A receptors to benzodiazepines. These phenomena may offer a novel explanation to why nicotine and alcohol are often co-abused.</description><identifier>ISSN: 0014-2999</identifier><identifier>EISSN: 1879-0712</identifier><identifier>DOI: 10.1016/j.ejphar.2006.10.056</identifier><identifier>PMID: 17141214</identifier><identifier>CODEN: EJPHAZ</identifier><language>eng</language><publisher>Amsterdam: Elsevier B.V</publisher><subject>Accumbens ; Animals ; Beroendelära ; Biological and medical sciences ; biosynthesis ; Central Nervous System Depressants ; Central Nervous System Depressants - pharmacokinetics ; Central Nervous System Depressants - pharmacology ; Corpus Striatum ; Corpus Striatum - drug effects ; Corpus Striatum - metabolism ; Diazepam ; Diazepam - pharmacology ; Dopamine ; Dopamine - biosynthesis ; drug effects ; Ethanol ; Ethanol - pharmacokinetics ; Ethanol - pharmacology ; Farmakologi och toxikologi ; GABA ; GABA [gamma-amino-butyric-acid] ; GABA Modulators ; GABA Modulators - pharmacology ; Hexamethonium ; Hexamethonium - pharmacology ; Male ; Medical sciences ; metabolism ; Neurosciences ; Neurovetenskaper ; Nicotine ; Nicotine - pharmacology ; Nicotinic Agonists ; Nicotinic Agonists - pharmacology ; Nicotinic Antagonists ; Nicotinic Antagonists - pharmacology ; Nucleus Accumbens ; Nucleus Accumbens - drug effects ; Nucleus Accumbens - metabolism ; pharmacokinetics ; pharmacology ; Pharmacology and Toxicology ; Pharmacology. Drug treatments ; Rat ; Rats ; Rats, Wistar ; Receptors ; Receptors, GABA - metabolism ; Substance Abuse ; Wistar</subject><ispartof>European journal of pharmacology, 2007-01, Vol.555 (2), p.139-147</ispartof><rights>2006 Elsevier B.V.</rights><rights>2007 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c427t-e935ea5a6c5da922d7926789b8864279ebeb88b6254ea74481e66cce66efffb83</citedby><cites>FETCH-LOGICAL-c427t-e935ea5a6c5da922d7926789b8864279ebeb88b6254ea74481e66cce66efffb83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18445954$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17141214$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://gup.ub.gu.se/publication/75440$$DView record from Swedish Publication Index$$Hfree_for_read</backlink></links><search><creatorcontrib>Löf, Elin</creatorcontrib><creatorcontrib>Chau, Pei Pei</creatorcontrib><creatorcontrib>Stomberg, Rosita</creatorcontrib><creatorcontrib>Söderpalm, Bo</creatorcontrib><title>Ethanol-induced dopamine elevation in the rat — Modulatory effects by subchronic treatment with nicotinic drugs</title><title>European journal of pharmacology</title><addtitle>Eur J Pharmacol</addtitle><description>Chronic nicotine administration is associated with increased ethanol consumption in laboratory animals and in humans. Some smokers report less sedation during acute ethanol intoxication after nicotine administration and the sedative effects from ethanol are mediated by inhibitory GABA
A-receptors. In a series of
in vivo microdialysis experiments we investigated whether subchronic pre-treatment with nicotinic drugs known to enhance ethanol consumption in the rat (nicotine or the peripheral nicotinic antagonist hexamethonium) could modulate the alterations in extracellular dopamine observed in response to administration of ethanol or the sedative GABA
A-agonist diazepam. In the nucleus accumbens and the dorsal striatum, systemic and/or local ethanol administration resulted in transient increases in extracellular dopamine levels that returned to baseline before the local levels of ethanol started to decline. In hexamethonium pre-treated rats, however, the nucleus accumbens dopamine levels were time-locked to the ethanol levels in the same area after systemic or local ethanol administration. Perfusion of diazepam into the nucleus accumbens produced a significant reduction in nucleus accumbens dopamine in controls. Prior subchronic treatment with nicotine or hexamethonium abolished this effect. The present results suggest that subchronic treatment with the nicotinic acetylcholine receptor antagonist hexamethonium reduces a GABA
A-R mediated counteraction of the nucleus accumbens dopamine response to ethanol. Additionally, we demonstrate that modulation of nicotinic receptors may reduce the sensitivity of GABA
A receptors to benzodiazepines. These phenomena may offer a novel explanation to why nicotine and alcohol are often co-abused.</description><subject>Accumbens</subject><subject>Animals</subject><subject>Beroendelära</subject><subject>Biological and medical sciences</subject><subject>biosynthesis</subject><subject>Central Nervous System Depressants</subject><subject>Central Nervous System Depressants - pharmacokinetics</subject><subject>Central Nervous System Depressants - pharmacology</subject><subject>Corpus Striatum</subject><subject>Corpus Striatum - drug effects</subject><subject>Corpus Striatum - metabolism</subject><subject>Diazepam</subject><subject>Diazepam - pharmacology</subject><subject>Dopamine</subject><subject>Dopamine - biosynthesis</subject><subject>drug effects</subject><subject>Ethanol</subject><subject>Ethanol - pharmacokinetics</subject><subject>Ethanol - pharmacology</subject><subject>Farmakologi och toxikologi</subject><subject>GABA</subject><subject>GABA [gamma-amino-butyric-acid]</subject><subject>GABA Modulators</subject><subject>GABA Modulators - pharmacology</subject><subject>Hexamethonium</subject><subject>Hexamethonium - pharmacology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>metabolism</subject><subject>Neurosciences</subject><subject>Neurovetenskaper</subject><subject>Nicotine</subject><subject>Nicotine - pharmacology</subject><subject>Nicotinic Agonists</subject><subject>Nicotinic Agonists - pharmacology</subject><subject>Nicotinic Antagonists</subject><subject>Nicotinic Antagonists - pharmacology</subject><subject>Nucleus Accumbens</subject><subject>Nucleus Accumbens - drug effects</subject><subject>Nucleus Accumbens - metabolism</subject><subject>pharmacokinetics</subject><subject>pharmacology</subject><subject>Pharmacology and Toxicology</subject><subject>Pharmacology. Drug treatments</subject><subject>Rat</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Receptors</subject><subject>Receptors, GABA - metabolism</subject><subject>Substance Abuse</subject><subject>Wistar</subject><issn>0014-2999</issn><issn>1879-0712</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><recordid>eNp9kc9u1DAQhyMEokvhDRDyBU7NYru2E1-QqqoFpCIucLYcZ7LxKmun_tNqbzwET8iT4CgreuNiWz9_MxrNV1VvCd4STMTH_Rb286jDlmIsSrTFXDyrNqRtZI0bQp9XG4wJq6mU8qx6FeMeY8wl5S-rM9IQRihhm-r-Jo3a-am2rs8GetT7WR-sAwQTPOhkvUPWoTQCCjqhP79-o2--z5NOPhwRDAOYFFF3RDF3ZgzeWYNSAJ0O4BJ6tGlEJfLJLh99yLv4unox6CnCm9N9Xv28vflx_aW--_756_XVXW0YbVIN8pKD5loY3mtJad9IKppWdm0rCiChg_LsBOUMdMNYS0AIY8pRhhq69vK8ulj7xkeYc6fmYA86HJXXVu3yrEq0yyqCajhjuOAfVnwO_j5DTOpgo4Fp0g58jkq0jFJJRAHZCprgYwww_OtMsFrMqL1azajFzJIWM6Xs3al_7g7QPxWdVBTg_QnQ0ehpCNoZG5-4ljEu-cJ9Wjkoy3uwEFQ0FlxxZ0ORoXpv_z_JXwrysc8</recordid><startdate>20070126</startdate><enddate>20070126</enddate><creator>Löf, Elin</creator><creator>Chau, Pei Pei</creator><creator>Stomberg, Rosita</creator><creator>Söderpalm, Bo</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>7X8</scope><scope>ADTPV</scope><scope>AOWAS</scope><scope>F1U</scope></search><sort><creationdate>20070126</creationdate><title>Ethanol-induced dopamine elevation in the rat — Modulatory effects by subchronic treatment with nicotinic drugs</title><author>Löf, Elin ; Chau, Pei Pei ; Stomberg, Rosita ; Söderpalm, Bo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c427t-e935ea5a6c5da922d7926789b8864279ebeb88b6254ea74481e66cce66efffb83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Accumbens</topic><topic>Animals</topic><topic>Beroendelära</topic><topic>Biological and medical sciences</topic><topic>biosynthesis</topic><topic>Central Nervous System Depressants</topic><topic>Central Nervous System Depressants - pharmacokinetics</topic><topic>Central Nervous System Depressants - pharmacology</topic><topic>Corpus Striatum</topic><topic>Corpus Striatum - drug effects</topic><topic>Corpus Striatum - metabolism</topic><topic>Diazepam</topic><topic>Diazepam - pharmacology</topic><topic>Dopamine</topic><topic>Dopamine - biosynthesis</topic><topic>drug effects</topic><topic>Ethanol</topic><topic>Ethanol - pharmacokinetics</topic><topic>Ethanol - pharmacology</topic><topic>Farmakologi och toxikologi</topic><topic>GABA</topic><topic>GABA [gamma-amino-butyric-acid]</topic><topic>GABA Modulators</topic><topic>GABA Modulators - pharmacology</topic><topic>Hexamethonium</topic><topic>Hexamethonium - pharmacology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>metabolism</topic><topic>Neurosciences</topic><topic>Neurovetenskaper</topic><topic>Nicotine</topic><topic>Nicotine - pharmacology</topic><topic>Nicotinic Agonists</topic><topic>Nicotinic Agonists - pharmacology</topic><topic>Nicotinic Antagonists</topic><topic>Nicotinic Antagonists - pharmacology</topic><topic>Nucleus Accumbens</topic><topic>Nucleus Accumbens - drug effects</topic><topic>Nucleus Accumbens - metabolism</topic><topic>pharmacokinetics</topic><topic>pharmacology</topic><topic>Pharmacology and Toxicology</topic><topic>Pharmacology. Drug treatments</topic><topic>Rat</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Receptors</topic><topic>Receptors, GABA - metabolism</topic><topic>Substance Abuse</topic><topic>Wistar</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Löf, Elin</creatorcontrib><creatorcontrib>Chau, Pei Pei</creatorcontrib><creatorcontrib>Stomberg, Rosita</creatorcontrib><creatorcontrib>Söderpalm, Bo</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><collection>SwePub</collection><collection>SwePub Articles</collection><collection>SWEPUB Göteborgs universitet</collection><jtitle>European journal of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Löf, Elin</au><au>Chau, Pei Pei</au><au>Stomberg, Rosita</au><au>Söderpalm, Bo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Ethanol-induced dopamine elevation in the rat — Modulatory effects by subchronic treatment with nicotinic drugs</atitle><jtitle>European journal of pharmacology</jtitle><addtitle>Eur J Pharmacol</addtitle><date>2007-01-26</date><risdate>2007</risdate><volume>555</volume><issue>2</issue><spage>139</spage><epage>147</epage><pages>139-147</pages><issn>0014-2999</issn><eissn>1879-0712</eissn><coden>EJPHAZ</coden><abstract>Chronic nicotine administration is associated with increased ethanol consumption in laboratory animals and in humans. Some smokers report less sedation during acute ethanol intoxication after nicotine administration and the sedative effects from ethanol are mediated by inhibitory GABA
A-receptors. In a series of
in vivo microdialysis experiments we investigated whether subchronic pre-treatment with nicotinic drugs known to enhance ethanol consumption in the rat (nicotine or the peripheral nicotinic antagonist hexamethonium) could modulate the alterations in extracellular dopamine observed in response to administration of ethanol or the sedative GABA
A-agonist diazepam. In the nucleus accumbens and the dorsal striatum, systemic and/or local ethanol administration resulted in transient increases in extracellular dopamine levels that returned to baseline before the local levels of ethanol started to decline. In hexamethonium pre-treated rats, however, the nucleus accumbens dopamine levels were time-locked to the ethanol levels in the same area after systemic or local ethanol administration. Perfusion of diazepam into the nucleus accumbens produced a significant reduction in nucleus accumbens dopamine in controls. Prior subchronic treatment with nicotine or hexamethonium abolished this effect. The present results suggest that subchronic treatment with the nicotinic acetylcholine receptor antagonist hexamethonium reduces a GABA
A-R mediated counteraction of the nucleus accumbens dopamine response to ethanol. Additionally, we demonstrate that modulation of nicotinic receptors may reduce the sensitivity of GABA
A receptors to benzodiazepines. These phenomena may offer a novel explanation to why nicotine and alcohol are often co-abused.</abstract><cop>Amsterdam</cop><pub>Elsevier B.V</pub><pmid>17141214</pmid><doi>10.1016/j.ejphar.2006.10.056</doi><tpages>9</tpages></addata></record> |
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| ispartof | European journal of pharmacology, 2007-01, Vol.555 (2), p.139-147 |
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| subjects | Accumbens Animals Beroendelära Biological and medical sciences biosynthesis Central Nervous System Depressants Central Nervous System Depressants - pharmacokinetics Central Nervous System Depressants - pharmacology Corpus Striatum Corpus Striatum - drug effects Corpus Striatum - metabolism Diazepam Diazepam - pharmacology Dopamine Dopamine - biosynthesis drug effects Ethanol Ethanol - pharmacokinetics Ethanol - pharmacology Farmakologi och toxikologi GABA GABA [gamma-amino-butyric-acid] GABA Modulators GABA Modulators - pharmacology Hexamethonium Hexamethonium - pharmacology Male Medical sciences metabolism Neurosciences Neurovetenskaper Nicotine Nicotine - pharmacology Nicotinic Agonists Nicotinic Agonists - pharmacology Nicotinic Antagonists Nicotinic Antagonists - pharmacology Nucleus Accumbens Nucleus Accumbens - drug effects Nucleus Accumbens - metabolism pharmacokinetics pharmacology Pharmacology and Toxicology Pharmacology. Drug treatments Rat Rats Rats, Wistar Receptors Receptors, GABA - metabolism Substance Abuse Wistar |
| title | Ethanol-induced dopamine elevation in the rat — Modulatory effects by subchronic treatment with nicotinic drugs |
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