Life events-induced decrease of corticosteroid type I receptors is associated with reduced corticosterone feedback and enhanced vulnerability to amphetamine self-administration.
Identifieur interne : 002062 ( Main/Corpus ); précédent : 002061; suivant : 002063Life events-induced decrease of corticosteroid type I receptors is associated with reduced corticosterone feedback and enhanced vulnerability to amphetamine self-administration.
Auteurs : S. Maccari ; P V Piazza ; J M Deminière ; V. Lemaire ; P. Mormède ; H. Simon ; L. Angelucci ; M. Le MoalSource :
- Brain research [ 0006-8993 ] ; 1991.
English descriptors
- KwdEn :
- Adrenalectomy (MeSH), Amphetamine (pharmacology), Animals (MeSH), Corticosterone (physiology), Environment (MeSH), Feedback (MeSH), Female (MeSH), Hippocampus (drug effects), Hippocampus (metabolism), Hypothalamo-Hypophyseal System (physiopathology), Male (MeSH), Pituitary-Adrenal System (physiopathology), Rats (MeSH), Rats, Inbred Strains (MeSH), Receptors, Glucocorticoid (metabolism), Self Administration (MeSH), Stress, Psychological (metabolism), Stress, Psychological (psychology).
- MESH :
- chemical , metabolism : Receptors, Glucocorticoid.
- chemical , pharmacology : Amphetamine.
- chemical , physiology : Corticosterone.
- drug effects : Hippocampus.
- metabolism : Hippocampus, Stress, Psychological.
- physiopathology : Hypothalamo-Hypophyseal System, Pituitary-Adrenal System.
- psychology : Stress, Psychological.
- Adrenalectomy, Animals, Environment, Feedback, Female, Male, Rats, Rats, Inbred Strains, Self Administration.
Abstract
In this study, we attempted to find out whether a social stress-induced increase in the vulnerability to acquire amphetamine self-administration was associated with a change in number of hippocampal corticosteroid receptors. This was examined in two types of sex-mixed colonies of rats. Animals were maintained for 4 weeks in: (1) 'stable social condition', membership did not change after constitution of the colony; (2) 'unstable social condition', the males were changed daily in a random design. The animals living in the 'stable social' conditions had: (1) a lower number of hippocampal type I corticosteroid receptors; (2) a longer duration of the increase in plasma corticosterone after exposure to novelty; (3) a higher vulnerability to acquire amphetamine self-administration. These findings suggest that a decrease in hippocampal type I corticosteroid receptors may be one of the biological mechanisms responsible for the impaired corticosterone feedback control observed in vulnerable animals. These findings throw more light on the role of hypothalamo-pituitary-adrenal axis in the modulation of adaptive behavior. The availability of drugs which are specific for corticosteroid receptors could represent a new approach to the therapy of certain behavioral disturbances.
DOI: 10.1016/0006-8993(91)90568-g
PubMed: 1860073
Links to Exploration step
pubmed:1860073Le document en format XML
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Lemaire</name></author><author><name sortKey="Mormede, P" sort="Mormede, P" uniqKey="Mormede P" first="P" last="Mormède">P. Mormède</name></author><author><name sortKey="Simon, H" sort="Simon, H" uniqKey="Simon H" first="H" last="Simon">H. Simon</name></author><author><name sortKey="Angelucci, L" sort="Angelucci, L" uniqKey="Angelucci L" first="L" last="Angelucci">L. Angelucci</name></author><author><name sortKey="Le Moal, M" sort="Le Moal, M" uniqKey="Le Moal M" first="M" last="Le Moal">M. Le Moal</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1991">1991</date><idno type="RBID">pubmed:1860073</idno><idno type="pmid">1860073</idno><idno type="doi">10.1016/0006-8993(91)90568-g</idno><idno type="wicri:Area/Main/Corpus">002062</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">002062</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Life events-induced decrease of corticosteroid type I receptors is associated with reduced corticosterone feedback and enhanced vulnerability to amphetamine self-administration.</title><author><name sortKey="Maccari, S" sort="Maccari, S" uniqKey="Maccari S" first="S" last="Maccari">S. Maccari</name><affiliation><nlm:affiliation>Laboratoire de Psychobiologie des Comportements Adaptatifs, INSERM U259, Bordeaux, France.</nlm:affiliation></affiliation></author><author><name sortKey="Piazza, P V" sort="Piazza, P V" uniqKey="Piazza P" first="P V" last="Piazza">P V Piazza</name></author><author><name sortKey="Deminiere, J M" sort="Deminiere, J M" uniqKey="Deminiere J" first="J M" last="Deminière">J M Deminière</name></author><author><name sortKey="Lemaire, V" sort="Lemaire, V" uniqKey="Lemaire V" first="V" last="Lemaire">V. Lemaire</name></author><author><name sortKey="Mormede, P" sort="Mormede, P" uniqKey="Mormede P" first="P" last="Mormède">P. Mormède</name></author><author><name sortKey="Simon, H" sort="Simon, H" uniqKey="Simon H" first="H" last="Simon">H. Simon</name></author><author><name sortKey="Angelucci, L" sort="Angelucci, L" uniqKey="Angelucci L" first="L" last="Angelucci">L. Angelucci</name></author><author><name sortKey="Le Moal, M" sort="Le Moal, M" uniqKey="Le Moal M" first="M" last="Le Moal">M. Le Moal</name></author></analytic><series><title level="j">Brain research</title><idno type="ISSN">0006-8993</idno><imprint><date when="1991" type="published">1991</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adrenalectomy (MeSH)</term><term>Amphetamine (pharmacology)</term><term>Animals (MeSH)</term><term>Corticosterone (physiology)</term><term>Environment (MeSH)</term><term>Feedback (MeSH)</term><term>Female (MeSH)</term><term>Hippocampus (drug effects)</term><term>Hippocampus (metabolism)</term><term>Hypothalamo-Hypophyseal System (physiopathology)</term><term>Male (MeSH)</term><term>Pituitary-Adrenal System (physiopathology)</term><term>Rats (MeSH)</term><term>Rats, Inbred Strains (MeSH)</term><term>Receptors, Glucocorticoid (metabolism)</term><term>Self Administration (MeSH)</term><term>Stress, Psychological (metabolism)</term><term>Stress, Psychological (psychology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Receptors, Glucocorticoid</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Amphetamine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="physiology" xml:lang="en"><term>Corticosterone</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Hippocampus</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Hippocampus</term><term>Stress, Psychological</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Hypothalamo-Hypophyseal System</term><term>Pituitary-Adrenal System</term></keywords><keywords scheme="MESH" qualifier="psychology" xml:lang="en"><term>Stress, Psychological</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adrenalectomy</term><term>Animals</term><term>Environment</term><term>Feedback</term><term>Female</term><term>Male</term><term>Rats</term><term>Rats, Inbred Strains</term><term>Self Administration</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">In this study, we attempted to find out whether a social stress-induced increase in the vulnerability to acquire amphetamine self-administration was associated with a change in number of hippocampal corticosteroid receptors. This was examined in two types of sex-mixed colonies of rats. Animals were maintained for 4 weeks in: (1) 'stable social condition', membership did not change after constitution of the colony; (2) 'unstable social condition', the males were changed daily in a random design. The animals living in the 'stable social' conditions had: (1) a lower number of hippocampal type I corticosteroid receptors; (2) a longer duration of the increase in plasma corticosterone after exposure to novelty; (3) a higher vulnerability to acquire amphetamine self-administration. These findings suggest that a decrease in hippocampal type I corticosteroid receptors may be one of the biological mechanisms responsible for the impaired corticosterone feedback control observed in vulnerable animals. These findings throw more light on the role of hypothalamo-pituitary-adrenal axis in the modulation of adaptive behavior. The availability of drugs which are specific for corticosteroid receptors could represent a new approach to the therapy of certain behavioral disturbances.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">1860073</PMID><DateCompleted><Year>1991</Year><Month>09</Month><Day>05</Day></DateCompleted><DateRevised><Year>2019</Year><Month>06</Month><Day>13</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0006-8993</ISSN><JournalIssue CitedMedium="Print"><Volume>547</Volume><Issue>1</Issue><PubDate><Year>1991</Year><Month>Apr</Month><Day>26</Day></PubDate></JournalIssue><Title>Brain research</Title><ISOAbbreviation>Brain Res</ISOAbbreviation></Journal><ArticleTitle>Life events-induced decrease of corticosteroid type I receptors is associated with reduced corticosterone feedback and enhanced vulnerability to amphetamine self-administration.</ArticleTitle><Pagination><MedlinePgn>7-12</MedlinePgn></Pagination><Abstract><AbstractText>In this study, we attempted to find out whether a social stress-induced increase in the vulnerability to acquire amphetamine self-administration was associated with a change in number of hippocampal corticosteroid receptors. This was examined in two types of sex-mixed colonies of rats. Animals were maintained for 4 weeks in: (1) 'stable social condition', membership did not change after constitution of the colony; (2) 'unstable social condition', the males were changed daily in a random design. The animals living in the 'stable social' conditions had: (1) a lower number of hippocampal type I corticosteroid receptors; (2) a longer duration of the increase in plasma corticosterone after exposure to novelty; (3) a higher vulnerability to acquire amphetamine self-administration. These findings suggest that a decrease in hippocampal type I corticosteroid receptors may be one of the biological mechanisms responsible for the impaired corticosterone feedback control observed in vulnerable animals. These findings throw more light on the role of hypothalamo-pituitary-adrenal axis in the modulation of adaptive behavior. The availability of drugs which are specific for corticosteroid receptors could represent a new approach to the therapy of certain behavioral disturbances.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Maccari</LastName><ForeName>S</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Laboratoire de Psychobiologie des Comportements Adaptatifs, INSERM U259, Bordeaux, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Piazza</LastName><ForeName>P V</ForeName><Initials>PV</Initials></Author><Author ValidYN="Y"><LastName>Deminière</LastName><ForeName>J M</ForeName><Initials>JM</Initials></Author><Author ValidYN="Y"><LastName>Lemaire</LastName><ForeName>V</ForeName><Initials>V</Initials></Author><Author ValidYN="Y"><LastName>Mormède</LastName><ForeName>P</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Simon</LastName><ForeName>H</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Angelucci</LastName><ForeName>L</ForeName><Initials>L</Initials></Author><Author ValidYN="Y"><LastName>Le Moal</LastName><ForeName>M</ForeName><Initials>M</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Brain Res</MedlineTA><NlmUniqueID>0045503</NlmUniqueID><ISSNLinking>0006-8993</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011965">Receptors, Glucocorticoid</NameOfSubstance></Chemical><Chemical><RegistryNumber>CK833KGX7E</RegistryNumber><NameOfSubstance UI="D000661">Amphetamine</NameOfSubstance></Chemical><Chemical><RegistryNumber>W980KJ009P</RegistryNumber><NameOfSubstance UI="D003345">Corticosterone</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000315" MajorTopicYN="N">Adrenalectomy</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000661" MajorTopicYN="N">Amphetamine</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003345" MajorTopicYN="N">Corticosterone</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004777" MajorTopicYN="N">Environment</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005246" MajorTopicYN="N">Feedback</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006624" MajorTopicYN="N">Hippocampus</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007030" MajorTopicYN="N">Hypothalamo-Hypophyseal System</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010913" MajorTopicYN="N">Pituitary-Adrenal System</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051381" MajorTopicYN="N">Rats</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011919" MajorTopicYN="N">Rats, Inbred Strains</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011965" MajorTopicYN="N">Receptors, Glucocorticoid</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012646" MajorTopicYN="N">Self Administration</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013315" MajorTopicYN="N">Stress, Psychological</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000523" MajorTopicYN="Y">psychology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1991</Year><Month>4</Month><Day>26</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1991</Year><Month>4</Month><Day>26</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1991</Year><Month>4</Month><Day>26</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId 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