Reduction in the anxiolytic effects of ethanol by centrally formed acetaldehyde: the role of catalase inhibitors and acetaldehyde-sequestering agents
Rationale Considerable evidence indicates that brain ethanol metabolism mediated by catalase is involved in modulating some of the behavioral and physiological effects of this drug, which suggests that the first metabolite of ethanol, acetaldehyde, may have central actions. Previous results have sho...
Gespeichert in:
| Veröffentlicht in: | Psychopharmacologia 2008-11, Vol.200 (4), p.455-464 |
|---|---|
| Hauptverfasser: | , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 464 |
|---|---|
| container_issue | 4 |
| container_start_page | 455 |
| container_title | Psychopharmacologia |
| container_volume | 200 |
| creator | Correa, M. Manrique, H. M. Font, L. Escrig, M. A. Aragon, C. M. G. |
| description | Rationale
Considerable evidence indicates that brain ethanol metabolism mediated by catalase is involved in modulating some of the behavioral and physiological effects of this drug, which suggests that the first metabolite of ethanol, acetaldehyde, may have central actions. Previous results have shown that acetaldehyde administered into the lateral ventricles produced anxiolysis in a novel open arena in rats.
Objectives
The present studies investigate the effects of centrally formed acetaldehyde on ethanol-induced anxiolysis.
Materials and methods
The effects of the catalase inhibitor sodium azide (SA; 0 or 10 mg/kg, IP) on ethanol-induced anxiolysis (0.0, 0.5, or 1.0 g/kg, IP) were evaluated in CD1 mice in two anxiety paradigms, the elevated plus maze and the dark/light box. Additional studies assessed the effect of the noncompetitive catalase inhibitor 3-amino-1,2,4-triazole (AT; 0.5 g/kg, IP) and the acetaldehyde inactivation agent
d
-penicillamine (50 mg/kg, IP) on the plus maze.
Results
SA reduced the anxiolytic effects of ethanol on several parameters evaluated in the elevated plus maze and in the dark/light box. In the plus maze, AT completely blocked and
d
-penicillamine significantly reduced the anxiolytic properties of ethanol.
Conclusions
Thus, when cerebral metabolism of ethanol into acetaldehyde is blocked by catalase inhibitors, or acetaldehyde is inactivated, there is a suppressive effect on the anxiolytic actions of ethanol. These data provide further support for the idea that centrally formed or administered acetaldehyde can contribute to some of the psychopharmacological actions of ethanol, including its anxiolytic properties. |
| doi_str_mv | 10.1007/s00213-008-1219-3 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_21046460</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>21046460</sourcerecordid><originalsourceid>FETCH-LOGICAL-c430t-6ee074fd32bb5c85a60694b4ceb14512c9ed8ec1cefb8ac27dbd17ed75d007d3</originalsourceid><addsrcrecordid>eNp1kU9rFTEUxYNY7LP6AdxIEOwuNf9mknEnxWqhUJDuh0xypy8lb_JMMtD5IH5fM30Pi4LZZJHfOffkHoTeMXrBKFWfMqWcCUKpJoyzjogXaMOk4IRTxV-iDaVCEMEafYpe5_xA65FavkKnTDdata3aoF8_wM22-DhhP-GyBWymRx_DUrzFMI5gS8ZxxFC2ZooBDwu2MJVkQljwGNMOHDYWigkOtouDz08eKQZYVdbUB5Ohem_94EtMufr_rSAZfs6QCyQ_3WNzX93zG3QympDh7fE-Q3dXX-8uv5Ob22_Xl19uiJWCFtICUCVHJ_gwNFY3pqVtJwdpYWCyYdx24DRYZmEctLFcucExBU41rq7PiTN0frDdp_iUod_5bCEEM0Gcc88Zla1saQU__AM-xDlNNVpldKca3ukKsQNkU8w5wdjvk9-ZtPSM9mtf_aGvvvbVr331omreH43noa7yWXEsqAIfj4DJ1oQxmcn6_Ifj9cNKiXU4P3B5v-4R0nPC_0__DfrTsQI</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>218975298</pqid></control><display><type>article</type><title>Reduction in the anxiolytic effects of ethanol by centrally formed acetaldehyde: the role of catalase inhibitors and acetaldehyde-sequestering agents</title><source>MEDLINE</source><source>SpringerLink Journals - AutoHoldings</source><creator>Correa, M. ; Manrique, H. M. ; Font, L. ; Escrig, M. A. ; Aragon, C. M. G.</creator><creatorcontrib>Correa, M. ; Manrique, H. M. ; Font, L. ; Escrig, M. A. ; Aragon, C. M. G.</creatorcontrib><description>Rationale
Considerable evidence indicates that brain ethanol metabolism mediated by catalase is involved in modulating some of the behavioral and physiological effects of this drug, which suggests that the first metabolite of ethanol, acetaldehyde, may have central actions. Previous results have shown that acetaldehyde administered into the lateral ventricles produced anxiolysis in a novel open arena in rats.
Objectives
The present studies investigate the effects of centrally formed acetaldehyde on ethanol-induced anxiolysis.
Materials and methods
The effects of the catalase inhibitor sodium azide (SA; 0 or 10 mg/kg, IP) on ethanol-induced anxiolysis (0.0, 0.5, or 1.0 g/kg, IP) were evaluated in CD1 mice in two anxiety paradigms, the elevated plus maze and the dark/light box. Additional studies assessed the effect of the noncompetitive catalase inhibitor 3-amino-1,2,4-triazole (AT; 0.5 g/kg, IP) and the acetaldehyde inactivation agent
d
-penicillamine (50 mg/kg, IP) on the plus maze.
Results
SA reduced the anxiolytic effects of ethanol on several parameters evaluated in the elevated plus maze and in the dark/light box. In the plus maze, AT completely blocked and
d
-penicillamine significantly reduced the anxiolytic properties of ethanol.
Conclusions
Thus, when cerebral metabolism of ethanol into acetaldehyde is blocked by catalase inhibitors, or acetaldehyde is inactivated, there is a suppressive effect on the anxiolytic actions of ethanol. These data provide further support for the idea that centrally formed or administered acetaldehyde can contribute to some of the psychopharmacological actions of ethanol, including its anxiolytic properties.</description><identifier>ISSN: 0033-3158</identifier><identifier>EISSN: 1432-2072</identifier><identifier>DOI: 10.1007/s00213-008-1219-3</identifier><identifier>PMID: 18587667</identifier><identifier>CODEN: PSYPAG</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer-Verlag</publisher><subject>Acetaldehyde - metabolism ; Alcoholism and acute alcohol poisoning ; Amitrole - pharmacology ; Animal behavior ; Animals ; Anti-Anxiety Agents - administration & dosage ; Anti-Anxiety Agents - pharmacology ; Anxiety ; Anxiety - drug therapy ; Biological and medical sciences ; Biomedical and Life Sciences ; Biomedicine ; Catalase - antagonists & inhibitors ; Central Nervous System Depressants - administration & dosage ; Central Nervous System Depressants - pharmacology ; Darkness ; Disease Models, Animal ; Dose-Response Relationship, Drug ; Enzymes ; Ethanol ; Ethanol - administration & dosage ; Ethanol - pharmacology ; Inhibitor drugs ; Light ; Male ; Maze Learning - drug effects ; Medical sciences ; Mice ; Neurosciences ; Original Investigation ; Pharmacology/Toxicology ; Psychiatry ; Psychopharmacology ; Rodents ; Sodium Azide - administration & dosage ; Sodium Azide - pharmacology ; Toxicology</subject><ispartof>Psychopharmacologia, 2008-11, Vol.200 (4), p.455-464</ispartof><rights>Springer-Verlag 2008</rights><rights>2008 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c430t-6ee074fd32bb5c85a60694b4ceb14512c9ed8ec1cefb8ac27dbd17ed75d007d3</citedby><cites>FETCH-LOGICAL-c430t-6ee074fd32bb5c85a60694b4ceb14512c9ed8ec1cefb8ac27dbd17ed75d007d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00213-008-1219-3$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00213-008-1219-3$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20697738$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18587667$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Correa, M.</creatorcontrib><creatorcontrib>Manrique, H. M.</creatorcontrib><creatorcontrib>Font, L.</creatorcontrib><creatorcontrib>Escrig, M. A.</creatorcontrib><creatorcontrib>Aragon, C. M. G.</creatorcontrib><title>Reduction in the anxiolytic effects of ethanol by centrally formed acetaldehyde: the role of catalase inhibitors and acetaldehyde-sequestering agents</title><title>Psychopharmacologia</title><addtitle>Psychopharmacology</addtitle><addtitle>Psychopharmacology (Berl)</addtitle><description>Rationale
Considerable evidence indicates that brain ethanol metabolism mediated by catalase is involved in modulating some of the behavioral and physiological effects of this drug, which suggests that the first metabolite of ethanol, acetaldehyde, may have central actions. Previous results have shown that acetaldehyde administered into the lateral ventricles produced anxiolysis in a novel open arena in rats.
Objectives
The present studies investigate the effects of centrally formed acetaldehyde on ethanol-induced anxiolysis.
Materials and methods
The effects of the catalase inhibitor sodium azide (SA; 0 or 10 mg/kg, IP) on ethanol-induced anxiolysis (0.0, 0.5, or 1.0 g/kg, IP) were evaluated in CD1 mice in two anxiety paradigms, the elevated plus maze and the dark/light box. Additional studies assessed the effect of the noncompetitive catalase inhibitor 3-amino-1,2,4-triazole (AT; 0.5 g/kg, IP) and the acetaldehyde inactivation agent
d
-penicillamine (50 mg/kg, IP) on the plus maze.
Results
SA reduced the anxiolytic effects of ethanol on several parameters evaluated in the elevated plus maze and in the dark/light box. In the plus maze, AT completely blocked and
d
-penicillamine significantly reduced the anxiolytic properties of ethanol.
Conclusions
Thus, when cerebral metabolism of ethanol into acetaldehyde is blocked by catalase inhibitors, or acetaldehyde is inactivated, there is a suppressive effect on the anxiolytic actions of ethanol. These data provide further support for the idea that centrally formed or administered acetaldehyde can contribute to some of the psychopharmacological actions of ethanol, including its anxiolytic properties.</description><subject>Acetaldehyde - metabolism</subject><subject>Alcoholism and acute alcohol poisoning</subject><subject>Amitrole - pharmacology</subject><subject>Animal behavior</subject><subject>Animals</subject><subject>Anti-Anxiety Agents - administration & dosage</subject><subject>Anti-Anxiety Agents - pharmacology</subject><subject>Anxiety</subject><subject>Anxiety - drug therapy</subject><subject>Biological and medical sciences</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Catalase - antagonists & inhibitors</subject><subject>Central Nervous System Depressants - administration & dosage</subject><subject>Central Nervous System Depressants - pharmacology</subject><subject>Darkness</subject><subject>Disease Models, Animal</subject><subject>Dose-Response Relationship, Drug</subject><subject>Enzymes</subject><subject>Ethanol</subject><subject>Ethanol - administration & dosage</subject><subject>Ethanol - pharmacology</subject><subject>Inhibitor drugs</subject><subject>Light</subject><subject>Male</subject><subject>Maze Learning - drug effects</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Neurosciences</subject><subject>Original Investigation</subject><subject>Pharmacology/Toxicology</subject><subject>Psychiatry</subject><subject>Psychopharmacology</subject><subject>Rodents</subject><subject>Sodium Azide - administration & dosage</subject><subject>Sodium Azide - pharmacology</subject><subject>Toxicology</subject><issn>0033-3158</issn><issn>1432-2072</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</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>eNp1kU9rFTEUxYNY7LP6AdxIEOwuNf9mknEnxWqhUJDuh0xypy8lb_JMMtD5IH5fM30Pi4LZZJHfOffkHoTeMXrBKFWfMqWcCUKpJoyzjogXaMOk4IRTxV-iDaVCEMEafYpe5_xA65FavkKnTDdata3aoF8_wM22-DhhP-GyBWymRx_DUrzFMI5gS8ZxxFC2ZooBDwu2MJVkQljwGNMOHDYWigkOtouDz08eKQZYVdbUB5Ohem_94EtMufr_rSAZfs6QCyQ_3WNzX93zG3QympDh7fE-Q3dXX-8uv5Ob22_Xl19uiJWCFtICUCVHJ_gwNFY3pqVtJwdpYWCyYdx24DRYZmEctLFcucExBU41rq7PiTN0frDdp_iUod_5bCEEM0Gcc88Zla1saQU__AM-xDlNNVpldKca3ukKsQNkU8w5wdjvk9-ZtPSM9mtf_aGvvvbVr331omreH43noa7yWXEsqAIfj4DJ1oQxmcn6_Ifj9cNKiXU4P3B5v-4R0nPC_0__DfrTsQI</recordid><startdate>20081101</startdate><enddate>20081101</enddate><creator>Correa, M.</creator><creator>Manrique, H. M.</creator><creator>Font, L.</creator><creator>Escrig, M. A.</creator><creator>Aragon, C. M. G.</creator><general>Springer-Verlag</general><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>AAYXX</scope><scope>CITATION</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></search><sort><creationdate>20081101</creationdate><title>Reduction in the anxiolytic effects of ethanol by centrally formed acetaldehyde: the role of catalase inhibitors and acetaldehyde-sequestering agents</title><author>Correa, M. ; Manrique, H. M. ; Font, L. ; Escrig, M. A. ; Aragon, C. M. G.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c430t-6ee074fd32bb5c85a60694b4ceb14512c9ed8ec1cefb8ac27dbd17ed75d007d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Acetaldehyde - metabolism</topic><topic>Alcoholism and acute alcohol poisoning</topic><topic>Amitrole - pharmacology</topic><topic>Animal behavior</topic><topic>Animals</topic><topic>Anti-Anxiety Agents - administration & dosage</topic><topic>Anti-Anxiety Agents - pharmacology</topic><topic>Anxiety</topic><topic>Anxiety - drug therapy</topic><topic>Biological and medical sciences</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Catalase - antagonists & inhibitors</topic><topic>Central Nervous System Depressants - administration & dosage</topic><topic>Central Nervous System Depressants - pharmacology</topic><topic>Darkness</topic><topic>Disease Models, Animal</topic><topic>Dose-Response Relationship, Drug</topic><topic>Enzymes</topic><topic>Ethanol</topic><topic>Ethanol - administration & dosage</topic><topic>Ethanol - pharmacology</topic><topic>Inhibitor drugs</topic><topic>Light</topic><topic>Male</topic><topic>Maze Learning - drug effects</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Neurosciences</topic><topic>Original Investigation</topic><topic>Pharmacology/Toxicology</topic><topic>Psychiatry</topic><topic>Psychopharmacology</topic><topic>Rodents</topic><topic>Sodium Azide - administration & dosage</topic><topic>Sodium Azide - pharmacology</topic><topic>Toxicology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Correa, M.</creatorcontrib><creatorcontrib>Manrique, H. M.</creatorcontrib><creatorcontrib>Font, L.</creatorcontrib><creatorcontrib>Escrig, M. A.</creatorcontrib><creatorcontrib>Aragon, C. M. 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>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Proquest Nursing & Allied Health Source</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</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 Edition)</collection><collection>ProQuest Central UK/Ireland</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>Medical Database</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><jtitle>Psychopharmacologia</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Correa, M.</au><au>Manrique, H. M.</au><au>Font, L.</au><au>Escrig, M. A.</au><au>Aragon, C. M. G.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Reduction in the anxiolytic effects of ethanol by centrally formed acetaldehyde: the role of catalase inhibitors and acetaldehyde-sequestering agents</atitle><jtitle>Psychopharmacologia</jtitle><stitle>Psychopharmacology</stitle><addtitle>Psychopharmacology (Berl)</addtitle><date>2008-11-01</date><risdate>2008</risdate><volume>200</volume><issue>4</issue><spage>455</spage><epage>464</epage><pages>455-464</pages><issn>0033-3158</issn><eissn>1432-2072</eissn><coden>PSYPAG</coden><abstract>Rationale
Considerable evidence indicates that brain ethanol metabolism mediated by catalase is involved in modulating some of the behavioral and physiological effects of this drug, which suggests that the first metabolite of ethanol, acetaldehyde, may have central actions. Previous results have shown that acetaldehyde administered into the lateral ventricles produced anxiolysis in a novel open arena in rats.
Objectives
The present studies investigate the effects of centrally formed acetaldehyde on ethanol-induced anxiolysis.
Materials and methods
The effects of the catalase inhibitor sodium azide (SA; 0 or 10 mg/kg, IP) on ethanol-induced anxiolysis (0.0, 0.5, or 1.0 g/kg, IP) were evaluated in CD1 mice in two anxiety paradigms, the elevated plus maze and the dark/light box. Additional studies assessed the effect of the noncompetitive catalase inhibitor 3-amino-1,2,4-triazole (AT; 0.5 g/kg, IP) and the acetaldehyde inactivation agent
d
-penicillamine (50 mg/kg, IP) on the plus maze.
Results
SA reduced the anxiolytic effects of ethanol on several parameters evaluated in the elevated plus maze and in the dark/light box. In the plus maze, AT completely blocked and
d
-penicillamine significantly reduced the anxiolytic properties of ethanol.
Conclusions
Thus, when cerebral metabolism of ethanol into acetaldehyde is blocked by catalase inhibitors, or acetaldehyde is inactivated, there is a suppressive effect on the anxiolytic actions of ethanol. These data provide further support for the idea that centrally formed or administered acetaldehyde can contribute to some of the psychopharmacological actions of ethanol, including its anxiolytic properties.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer-Verlag</pub><pmid>18587667</pmid><doi>10.1007/s00213-008-1219-3</doi><tpages>10</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0033-3158 |
| ispartof | Psychopharmacologia, 2008-11, Vol.200 (4), p.455-464 |
| issn | 0033-3158 1432-2072 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_21046460 |
| source | MEDLINE; SpringerLink Journals - AutoHoldings |
| subjects | Acetaldehyde - metabolism Alcoholism and acute alcohol poisoning Amitrole - pharmacology Animal behavior Animals Anti-Anxiety Agents - administration & dosage Anti-Anxiety Agents - pharmacology Anxiety Anxiety - drug therapy Biological and medical sciences Biomedical and Life Sciences Biomedicine Catalase - antagonists & inhibitors Central Nervous System Depressants - administration & dosage Central Nervous System Depressants - pharmacology Darkness Disease Models, Animal Dose-Response Relationship, Drug Enzymes Ethanol Ethanol - administration & dosage Ethanol - pharmacology Inhibitor drugs Light Male Maze Learning - drug effects Medical sciences Mice Neurosciences Original Investigation Pharmacology/Toxicology Psychiatry Psychopharmacology Rodents Sodium Azide - administration & dosage Sodium Azide - pharmacology Toxicology |
| title | Reduction in the anxiolytic effects of ethanol by centrally formed acetaldehyde: the role of catalase inhibitors and acetaldehyde-sequestering agents |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-06T20%3A45%3A30IST&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=Reduction%20in%20the%20anxiolytic%20effects%20of%20ethanol%20by%20centrally%20formed%20acetaldehyde:%20the%20role%20of%20catalase%20inhibitors%20and%20acetaldehyde-sequestering%20agents&rft.jtitle=Psychopharmacologia&rft.au=Correa,%20M.&rft.date=2008-11-01&rft.volume=200&rft.issue=4&rft.spage=455&rft.epage=464&rft.pages=455-464&rft.issn=0033-3158&rft.eissn=1432-2072&rft.coden=PSYPAG&rft_id=info:doi/10.1007/s00213-008-1219-3&rft_dat=%3Cproquest_cross%3E21046460%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=218975298&rft_id=info:pmid/18587667&rfr_iscdi=true |