Corticosteroids operate as a switch between memory systems.
Identifieur interne : 000531 ( PubMed/Checkpoint ); précédent : 000530; suivant : 000532Corticosteroids operate as a switch between memory systems.
Auteurs : Lars Schwabe [Allemagne] ; Hartmut Sch Chinger ; E Ron De Kloet ; Melly S. OitzlSource :
- Journal of cognitive neuroscience [ 1530-8898 ] ; 2010.
English descriptors
- KwdEn :
- Animals, Caudate Nucleus (physiology), Corticosterone (pharmacology), Corticosterone (physiology), Hippocampus (physiology), Memory (drug effects), Memory (physiology), Mice, Mineralocorticoid Receptor Antagonists (pharmacology), Mineralocorticoids (metabolism), Receptors, Mineralocorticoid (physiology), Spironolactone (analogs & derivatives), Spironolactone (pharmacology), Stress, Physiological (physiology).
- MESH :
- chemical , analogs & derivatives : Spironolactone.
- chemical , metabolism : Mineralocorticoids.
- chemical , pharmacology : Corticosterone, Mineralocorticoid Receptor Antagonists, Spironolactone.
- drug effects : Memory.
- physiology : Caudate Nucleus, Corticosterone, Hippocampus, Memory, Receptors, Mineralocorticoid, Stress, Physiological.
- Animals, Mice.
Abstract
Stress and corticosteroid hormones are known to affect learning and memory processes. In this study, we examined whether stress and corticosteroids are capable of facilitating the switch between multiple memory systems in mice. For this purpose, we designed a task that allowed measurement of nucleus caudate-based stimulus-response and hippocampus-based spatial learning strategies. Naive mice used spatial strategies to locate an exit hole on a circular hole board at a fixed location flagged by a proximal stimulus. When the mice were either stressed or administered corticosterone before the task, 30-50% of the mice switched to a stimulus-response strategy. This switch between learning strategies was accompanied by a rescue of performance, whereas performance declined in the stressed mice that kept using the spatial strategy. Pretreatment with a mineralocorticoid receptor antagonist prevented the switch toward the stimulus-response strategy but led to deterioration of hippocampus-dependent performance. These findings (i) show that corticosteroids promote the transition from spatial to stimulus-response memory systems, (ii) provide evidence that the mineralocorticoid receptor underlies this corticosteroid-mediated switch, and (iii) suggest that a stress-induced switch from hippocampus-based to nucleus caudate-based memory systems can rescue performance.
DOI: 10.1162/jocn.2009.21278
PubMed: 19445601
Affiliations:
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Lars.Schwabe@rub.de</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>University of Trier</wicri:regionArea></affiliation></author><author><name sortKey="Sch Chinger, Hartmut" sort="Sch Chinger, Hartmut" uniqKey="Sch Chinger H" first="Hartmut" last="Sch Chinger">Hartmut Sch Chinger</name></author><author><name sortKey="De Kloet, E Ron" sort="De Kloet, E Ron" uniqKey="De Kloet E" first="E Ron" last="De Kloet">E Ron De Kloet</name></author><author><name sortKey="Oitzl, Melly S" sort="Oitzl, Melly S" uniqKey="Oitzl M" first="Melly S" last="Oitzl">Melly S. Oitzl</name></author></analytic><series><title level="j">Journal of cognitive neuroscience</title><idno type="eISSN">1530-8898</idno><imprint><date when="2010" type="published">2010</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Caudate Nucleus (physiology)</term><term>Corticosterone (pharmacology)</term><term>Corticosterone (physiology)</term><term>Hippocampus (physiology)</term><term>Memory (drug effects)</term><term>Memory (physiology)</term><term>Mice</term><term>Mineralocorticoid Receptor Antagonists (pharmacology)</term><term>Mineralocorticoids (metabolism)</term><term>Receptors, Mineralocorticoid (physiology)</term><term>Spironolactone (analogs & derivatives)</term><term>Spironolactone (pharmacology)</term><term>Stress, Physiological (physiology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Spironolactone</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Mineralocorticoids</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Corticosterone</term><term>Mineralocorticoid Receptor Antagonists</term><term>Spironolactone</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Memory</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Caudate Nucleus</term><term>Corticosterone</term><term>Hippocampus</term><term>Memory</term><term>Receptors, Mineralocorticoid</term><term>Stress, Physiological</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Mice</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Stress and corticosteroid hormones are known to affect learning and memory processes. In this study, we examined whether stress and corticosteroids are capable of facilitating the switch between multiple memory systems in mice. For this purpose, we designed a task that allowed measurement of nucleus caudate-based stimulus-response and hippocampus-based spatial learning strategies. Naive mice used spatial strategies to locate an exit hole on a circular hole board at a fixed location flagged by a proximal stimulus. When the mice were either stressed or administered corticosterone before the task, 30-50% of the mice switched to a stimulus-response strategy. This switch between learning strategies was accompanied by a rescue of performance, whereas performance declined in the stressed mice that kept using the spatial strategy. Pretreatment with a mineralocorticoid receptor antagonist prevented the switch toward the stimulus-response strategy but led to deterioration of hippocampus-dependent performance. These findings (i) show that corticosteroids promote the transition from spatial to stimulus-response memory systems, (ii) provide evidence that the mineralocorticoid receptor underlies this corticosteroid-mediated switch, and (iii) suggest that a stress-induced switch from hippocampus-based to nucleus caudate-based memory systems can rescue performance.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">19445601</PMID><DateCreated><Year>2010</Year><Month>04</Month><Day>06</Day></DateCreated><DateCompleted><Year>2010</Year><Month>08</Month><Day>12</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1530-8898</ISSN><JournalIssue CitedMedium="Internet"><Volume>22</Volume><Issue>7</Issue><PubDate><Year>2010</Year><Month>Jul</Month></PubDate></JournalIssue><Title>Journal of cognitive neuroscience</Title><ISOAbbreviation>J Cogn Neurosci</ISOAbbreviation></Journal><ArticleTitle>Corticosteroids operate as a switch between memory systems.</ArticleTitle><Pagination><MedlinePgn>1362-72</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1162/jocn.2009.21278</ELocationID><Abstract><AbstractText>Stress and corticosteroid hormones are known to affect learning and memory processes. In this study, we examined whether stress and corticosteroids are capable of facilitating the switch between multiple memory systems in mice. For this purpose, we designed a task that allowed measurement of nucleus caudate-based stimulus-response and hippocampus-based spatial learning strategies. Naive mice used spatial strategies to locate an exit hole on a circular hole board at a fixed location flagged by a proximal stimulus. When the mice were either stressed or administered corticosterone before the task, 30-50% of the mice switched to a stimulus-response strategy. This switch between learning strategies was accompanied by a rescue of performance, whereas performance declined in the stressed mice that kept using the spatial strategy. Pretreatment with a mineralocorticoid receptor antagonist prevented the switch toward the stimulus-response strategy but led to deterioration of hippocampus-dependent performance. These findings (i) show that corticosteroids promote the transition from spatial to stimulus-response memory systems, (ii) provide evidence that the mineralocorticoid receptor underlies this corticosteroid-mediated switch, and (iii) suggest that a stress-induced switch from hippocampus-based to nucleus caudate-based memory systems can rescue performance.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Schwabe</LastName><ForeName>Lars</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>University of Trier, Germany. Lars.Schwabe@rub.de</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Schächinger</LastName><ForeName>Hartmut</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>de Kloet</LastName><ForeName>E Ron</ForeName><Initials>ER</Initials></Author><Author ValidYN="Y"><LastName>Oitzl</LastName><ForeName>Melly S</ForeName><Initials>MS</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>United States</Country><MedlineTA>J Cogn Neurosci</MedlineTA><NlmUniqueID>8910747</NlmUniqueID><ISSNLinking>0898-929X</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000451">Mineralocorticoid Receptor Antagonists</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D008901">Mineralocorticoids</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018161">Receptors, Mineralocorticoid</NameOfSubstance></Chemical><Chemical><RegistryNumber>27O7W4T232</RegistryNumber><NameOfSubstance UI="D013148">Spironolactone</NameOfSubstance></Chemical><Chemical><RegistryNumber>76676-34-1</RegistryNumber><NameOfSubstance UI="C041006">RU 28318</NameOfSubstance></Chemical><Chemical><RegistryNumber>W980KJ009P</RegistryNumber><NameOfSubstance UI="D003345">Corticosterone</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002421" MajorTopicYN="N">Caudate Nucleus</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003345" MajorTopicYN="Y">Corticosterone</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName><QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006624" MajorTopicYN="N">Hippocampus</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008568" MajorTopicYN="N">Memory</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000451" MajorTopicYN="N">Mineralocorticoid Receptor Antagonists</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008901" MajorTopicYN="N">Mineralocorticoids</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018161" MajorTopicYN="N">Receptors, Mineralocorticoid</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013148" MajorTopicYN="N">Spironolactone</DescriptorName><QualifierName UI="Q000031" MajorTopicYN="N">analogs & derivatives</QualifierName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013312" MajorTopicYN="N">Stress, Physiological</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2009</Year><Month>5</Month><Day>19</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2009</Year><Month>5</Month><Day>19</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2010</Year><Month>8</Month><Day>13</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">19445601</ArticleId><ArticleId IdType="doi">10.1162/jocn.2009.21278</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Allemagne</li></country></list><tree><noCountry><name sortKey="De Kloet, E Ron" sort="De Kloet, E Ron" uniqKey="De Kloet E" first="E Ron" last="De Kloet">E Ron De Kloet</name><name sortKey="Oitzl, Melly S" sort="Oitzl, Melly S" uniqKey="Oitzl M" first="Melly S" last="Oitzl">Melly S. Oitzl</name><name sortKey="Sch Chinger, Hartmut" sort="Sch Chinger, Hartmut" uniqKey="Sch Chinger H" first="Hartmut" last="Sch Chinger">Hartmut Sch Chinger</name></noCountry><country name="Allemagne"><noRegion><name sortKey="Schwabe, Lars" sort="Schwabe, Lars" uniqKey="Schwabe L" first="Lars" last="Schwabe">Lars Schwabe</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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