Ethanol-Sensitive Brain Regions in Rat and Mouse: A Cartographic Review, Using Immediate Early Gene Expression
Background: Ethanol addiction has been conceptualized as a progression from occasional, impulsive use to compulsive behavior. Ethanol‐dependence is a chronic pathology with repeated cycles of withdrawal, craving, and relapse. Specific molecular and cellular mechanisms underlie these transition stag...
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description | Background: Ethanol addiction has been conceptualized as a progression from occasional, impulsive use to compulsive behavior. Ethanol‐dependence is a chronic pathology with repeated cycles of withdrawal, craving, and relapse. Specific molecular and cellular mechanisms underlie these transition stages.
Methods: This review aimed at elucidating whether there are also adaptations in the pattern of brain regions responding to ethanol. This paper reviews the evidence in rodents for activation of specific brain regions, assessed by induction of IEG expression, following acute and chronic ethanol exposure.
Results: The review sheds light on the specific patterns of response in regions of the brain to different types of ethanol exposure and shows that activation of specific brain regions may occur in particular phases of the development of ethanol addiction. Some brain regions respond consistently following acute or chronic treatments or withdrawal: the prefrontal cortex; nucleus accumbens; lateral septum; hippocampus; perioculomotor urocortin‐containing cells population (pIIIu), also known as Edinger‐Westphal nucleus; central nucleus of the amygdale; and the paraventricular nucleus of hypothalamus. The two last brain areas are particularly activated by relapse‐inducing stressors. It is of interest that the amygdala, hippocampus, and prefrontal cortex, which belong to the reward system, are activated by cue‐induced relapse to ethanol self‐administration in rodents and humans, while activation of these regions is reversed with anticraving compounds. Following chronic exposure, IEG induction desensitizes while withdrawal reactivates these regions.
Discussion: Some responding regions are implicated in reward related processes (VTA, extended amygdala, hypothalamus, hippocampus, prelimbic cortex, ventral part of lateral septum) and some others in aversive‐related processes (area postrema, nucleus of solitary tract).
Conclusion: A better understanding of the neural circuits affected by ethanol and their adaptations during the development of ethanol addiction will provide new opportunities for developing appropriate therapies. |
doi_str_mv | 10.1111/j.1530-0277.2009.00916.x |
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Methods: This review aimed at elucidating whether there are also adaptations in the pattern of brain regions responding to ethanol. This paper reviews the evidence in rodents for activation of specific brain regions, assessed by induction of IEG expression, following acute and chronic ethanol exposure.
Results: The review sheds light on the specific patterns of response in regions of the brain to different types of ethanol exposure and shows that activation of specific brain regions may occur in particular phases of the development of ethanol addiction. Some brain regions respond consistently following acute or chronic treatments or withdrawal: the prefrontal cortex; nucleus accumbens; lateral septum; hippocampus; perioculomotor urocortin‐containing cells population (pIIIu), also known as Edinger‐Westphal nucleus; central nucleus of the amygdale; and the paraventricular nucleus of hypothalamus. The two last brain areas are particularly activated by relapse‐inducing stressors. It is of interest that the amygdala, hippocampus, and prefrontal cortex, which belong to the reward system, are activated by cue‐induced relapse to ethanol self‐administration in rodents and humans, while activation of these regions is reversed with anticraving compounds. Following chronic exposure, IEG induction desensitizes while withdrawal reactivates these regions.
Discussion: Some responding regions are implicated in reward related processes (VTA, extended amygdala, hypothalamus, hippocampus, prelimbic cortex, ventral part of lateral septum) and some others in aversive‐related processes (area postrema, nucleus of solitary tract).
Conclusion: A better understanding of the neural circuits affected by ethanol and their adaptations during the development of ethanol addiction will provide new opportunities for developing appropriate therapies.</description><identifier>ISSN: 0145-6008</identifier><identifier>EISSN: 1530-0277</identifier><identifier>DOI: 10.1111/j.1530-0277.2009.00916.x</identifier><identifier>PMID: 19302091</identifier><identifier>CODEN: ACRSDM</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Alcoholism ; Alcoholism - genetics ; Alcoholism - metabolism ; Alcoholism - pathology ; Alcoholism and acute alcohol poisoning ; Animals ; Biological and medical sciences ; Brain ; Brain - metabolism ; Brain - pathology ; c-Fos ; Central Nervous System Depressants ; Central Nervous System Depressants - pharmacology ; Disease Models, Animal ; Dose-Response Relationship, Drug ; Egr-1 ; Ethanol ; Ethanol - pharmacology ; Extended Amygdala ; Female ; Gene Expression Regulation ; Gene Expression Regulation - drug effects ; Genes, Immediate-Early ; Genes, Immediate-Early - genetics ; Immediate Early Gene ; Life Sciences ; Male ; Medical sciences ; Mesolimbic Dopamine Circuitry ; Mice ; Mice, Inbred C57BL ; Mice, Inbred DBA ; Neurons and Cognition ; Rats ; Rats, Sprague-Dawley ; Rats, Wistar ; Toxicology</subject><ispartof>Alcoholism, clinical and experimental research, 2009-06, Vol.33 (6), p.945-969</ispartof><rights>Copyright © 2009 by the Research Society on Alcoholism</rights><rights>2009 INIST-CNRS</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5696-e6084a81638e6b4c6071aa14068a0abd89cb4172afb2a472bccd0ec19d570373</citedby><cites>FETCH-LOGICAL-c5696-e6084a81638e6b4c6071aa14068a0abd89cb4172afb2a472bccd0ec19d570373</cites><orcidid>0000-0002-9812-3791 ; 0000-0002-9788-0918 ; 0000-0003-1427-9332 ; 0000-0003-2462-2878</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1530-0277.2009.00916.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1530-0277.2009.00916.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>230,314,780,784,885,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=21658856$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19302091$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://inserm.hal.science/inserm-00746168$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Vilpoux, Catherine</creatorcontrib><creatorcontrib>Warnault, Vincent</creatorcontrib><creatorcontrib>Pierrefiche, Olivier</creatorcontrib><creatorcontrib>Daoust, Martine</creatorcontrib><creatorcontrib>Naassila, Mickael</creatorcontrib><title>Ethanol-Sensitive Brain Regions in Rat and Mouse: A Cartographic Review, Using Immediate Early Gene Expression</title><title>Alcoholism, clinical and experimental research</title><addtitle>Alcohol Clin Exp Res</addtitle><description>Background: Ethanol addiction has been conceptualized as a progression from occasional, impulsive use to compulsive behavior. Ethanol‐dependence is a chronic pathology with repeated cycles of withdrawal, craving, and relapse. Specific molecular and cellular mechanisms underlie these transition stages.
Methods: This review aimed at elucidating whether there are also adaptations in the pattern of brain regions responding to ethanol. This paper reviews the evidence in rodents for activation of specific brain regions, assessed by induction of IEG expression, following acute and chronic ethanol exposure.
Results: The review sheds light on the specific patterns of response in regions of the brain to different types of ethanol exposure and shows that activation of specific brain regions may occur in particular phases of the development of ethanol addiction. Some brain regions respond consistently following acute or chronic treatments or withdrawal: the prefrontal cortex; nucleus accumbens; lateral septum; hippocampus; perioculomotor urocortin‐containing cells population (pIIIu), also known as Edinger‐Westphal nucleus; central nucleus of the amygdale; and the paraventricular nucleus of hypothalamus. The two last brain areas are particularly activated by relapse‐inducing stressors. It is of interest that the amygdala, hippocampus, and prefrontal cortex, which belong to the reward system, are activated by cue‐induced relapse to ethanol self‐administration in rodents and humans, while activation of these regions is reversed with anticraving compounds. Following chronic exposure, IEG induction desensitizes while withdrawal reactivates these regions.
Discussion: Some responding regions are implicated in reward related processes (VTA, extended amygdala, hypothalamus, hippocampus, prelimbic cortex, ventral part of lateral septum) and some others in aversive‐related processes (area postrema, nucleus of solitary tract).
Conclusion: A better understanding of the neural circuits affected by ethanol and their adaptations during the development of ethanol addiction will provide new opportunities for developing appropriate therapies.</description><subject>Alcoholism</subject><subject>Alcoholism - genetics</subject><subject>Alcoholism - metabolism</subject><subject>Alcoholism - pathology</subject><subject>Alcoholism and acute alcohol poisoning</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Brain</subject><subject>Brain - metabolism</subject><subject>Brain - pathology</subject><subject>c-Fos</subject><subject>Central Nervous System Depressants</subject><subject>Central Nervous System Depressants - pharmacology</subject><subject>Disease Models, Animal</subject><subject>Dose-Response Relationship, Drug</subject><subject>Egr-1</subject><subject>Ethanol</subject><subject>Ethanol - pharmacology</subject><subject>Extended Amygdala</subject><subject>Female</subject><subject>Gene Expression Regulation</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Genes, Immediate-Early</subject><subject>Genes, Immediate-Early - genetics</subject><subject>Immediate Early Gene</subject><subject>Life Sciences</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mesolimbic Dopamine Circuitry</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Inbred DBA</subject><subject>Neurons and Cognition</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Rats, Wistar</subject><subject>Toxicology</subject><issn>0145-6008</issn><issn>1530-0277</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkU-P0zAQxSMEYsvCV0C-wGmTHeeP7SJxKFW3XamAWIr2aE1ct3VJnGKn3fbb42yqcsWS5ZH8e2_GflFEKCQ0rNttQosMYkg5T1KAYRI2ZcnxRTS4XLyMBkDzImYA4ip64_0WAHLB2Ovoig4zSINkENlJu0HbVPFPbb1pzUGTLw6NJQ96bRrrSVdiS9Auyddm7_UnMiJjdG2zdrjbGBXAg9FPN-SXN3ZN7utaLw22mkzQVScy1TaUx53T3ge_t9GrFVZevzuf19HibrIYz-L59-n9eDSPVcGGLNYMRI6CskxoVuaKAaeINAcmELBciqEqc8pTXJUp5jwtlVqCVnS4LDhkPLuObnrbDVZy50yN7iQbNHI2mktjvXa1BOA5o0wcaMA_9vjONX_22reyNl7pqkKrw5tlCoyF3h0oelC5xnunVxdzCrJLRm5lF4DsApBdMvI5GXkM0vfnHvsyfNE_4TmKAHw4A-gVViuHVhl_4VLKCiEKFrjPPfdkKn367wHkaDx5CFXQx73e-FYfL3p0vyXjGS_k47epvJstskf-I5WL7C92Wrdi</recordid><startdate>200906</startdate><enddate>200906</enddate><creator>Vilpoux, Catherine</creator><creator>Warnault, Vincent</creator><creator>Pierrefiche, Olivier</creator><creator>Daoust, Martine</creator><creator>Naassila, Mickael</creator><general>Blackwell Publishing Ltd</general><general>Wiley</general><scope>BSCLL</scope><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>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>1XC</scope><orcidid>https://orcid.org/0000-0002-9812-3791</orcidid><orcidid>https://orcid.org/0000-0002-9788-0918</orcidid><orcidid>https://orcid.org/0000-0003-1427-9332</orcidid><orcidid>https://orcid.org/0000-0003-2462-2878</orcidid></search><sort><creationdate>200906</creationdate><title>Ethanol-Sensitive Brain Regions in Rat and Mouse: A Cartographic Review, Using Immediate Early Gene Expression</title><author>Vilpoux, Catherine ; Warnault, Vincent ; Pierrefiche, Olivier ; Daoust, Martine ; Naassila, Mickael</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5696-e6084a81638e6b4c6071aa14068a0abd89cb4172afb2a472bccd0ec19d570373</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Alcoholism</topic><topic>Alcoholism - genetics</topic><topic>Alcoholism - metabolism</topic><topic>Alcoholism - pathology</topic><topic>Alcoholism and acute alcohol poisoning</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Brain</topic><topic>Brain - metabolism</topic><topic>Brain - pathology</topic><topic>c-Fos</topic><topic>Central Nervous System Depressants</topic><topic>Central Nervous System Depressants - pharmacology</topic><topic>Disease Models, Animal</topic><topic>Dose-Response Relationship, Drug</topic><topic>Egr-1</topic><topic>Ethanol</topic><topic>Ethanol - pharmacology</topic><topic>Extended Amygdala</topic><topic>Female</topic><topic>Gene Expression Regulation</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Genes, Immediate-Early</topic><topic>Genes, Immediate-Early - genetics</topic><topic>Immediate Early Gene</topic><topic>Life Sciences</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Mesolimbic Dopamine Circuitry</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Inbred DBA</topic><topic>Neurons and Cognition</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Rats, Wistar</topic><topic>Toxicology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Vilpoux, Catherine</creatorcontrib><creatorcontrib>Warnault, Vincent</creatorcontrib><creatorcontrib>Pierrefiche, Olivier</creatorcontrib><creatorcontrib>Daoust, Martine</creatorcontrib><creatorcontrib>Naassila, Mickael</creatorcontrib><collection>Istex</collection><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>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>Hyper Article en Ligne (HAL)</collection><jtitle>Alcoholism, clinical and experimental research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Vilpoux, Catherine</au><au>Warnault, Vincent</au><au>Pierrefiche, Olivier</au><au>Daoust, Martine</au><au>Naassila, Mickael</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Ethanol-Sensitive Brain Regions in Rat and Mouse: A Cartographic Review, Using Immediate Early Gene Expression</atitle><jtitle>Alcoholism, clinical and experimental research</jtitle><addtitle>Alcohol Clin Exp Res</addtitle><date>2009-06</date><risdate>2009</risdate><volume>33</volume><issue>6</issue><spage>945</spage><epage>969</epage><pages>945-969</pages><issn>0145-6008</issn><eissn>1530-0277</eissn><coden>ACRSDM</coden><abstract>Background: Ethanol addiction has been conceptualized as a progression from occasional, impulsive use to compulsive behavior. Ethanol‐dependence is a chronic pathology with repeated cycles of withdrawal, craving, and relapse. Specific molecular and cellular mechanisms underlie these transition stages.
Methods: This review aimed at elucidating whether there are also adaptations in the pattern of brain regions responding to ethanol. This paper reviews the evidence in rodents for activation of specific brain regions, assessed by induction of IEG expression, following acute and chronic ethanol exposure.
Results: The review sheds light on the specific patterns of response in regions of the brain to different types of ethanol exposure and shows that activation of specific brain regions may occur in particular phases of the development of ethanol addiction. Some brain regions respond consistently following acute or chronic treatments or withdrawal: the prefrontal cortex; nucleus accumbens; lateral septum; hippocampus; perioculomotor urocortin‐containing cells population (pIIIu), also known as Edinger‐Westphal nucleus; central nucleus of the amygdale; and the paraventricular nucleus of hypothalamus. The two last brain areas are particularly activated by relapse‐inducing stressors. It is of interest that the amygdala, hippocampus, and prefrontal cortex, which belong to the reward system, are activated by cue‐induced relapse to ethanol self‐administration in rodents and humans, while activation of these regions is reversed with anticraving compounds. Following chronic exposure, IEG induction desensitizes while withdrawal reactivates these regions.
Discussion: Some responding regions are implicated in reward related processes (VTA, extended amygdala, hypothalamus, hippocampus, prelimbic cortex, ventral part of lateral septum) and some others in aversive‐related processes (area postrema, nucleus of solitary tract).
Conclusion: A better understanding of the neural circuits affected by ethanol and their adaptations during the development of ethanol addiction will provide new opportunities for developing appropriate therapies.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>19302091</pmid><doi>10.1111/j.1530-0277.2009.00916.x</doi><tpages>25</tpages><orcidid>https://orcid.org/0000-0002-9812-3791</orcidid><orcidid>https://orcid.org/0000-0002-9788-0918</orcidid><orcidid>https://orcid.org/0000-0003-1427-9332</orcidid><orcidid>https://orcid.org/0000-0003-2462-2878</orcidid></addata></record> |
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subjects | Alcoholism Alcoholism - genetics Alcoholism - metabolism Alcoholism - pathology Alcoholism and acute alcohol poisoning Animals Biological and medical sciences Brain Brain - metabolism Brain - pathology c-Fos Central Nervous System Depressants Central Nervous System Depressants - pharmacology Disease Models, Animal Dose-Response Relationship, Drug Egr-1 Ethanol Ethanol - pharmacology Extended Amygdala Female Gene Expression Regulation Gene Expression Regulation - drug effects Genes, Immediate-Early Genes, Immediate-Early - genetics Immediate Early Gene Life Sciences Male Medical sciences Mesolimbic Dopamine Circuitry Mice Mice, Inbred C57BL Mice, Inbred DBA Neurons and Cognition Rats Rats, Sprague-Dawley Rats, Wistar Toxicology |
title | Ethanol-Sensitive Brain Regions in Rat and Mouse: A Cartographic Review, Using Immediate Early Gene Expression |
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