Mifepristone and spironolactone differently alter cocaine intravenous self-administration and cocaine-induced locomotion in C57BL/6J mice.
Identifieur interne : 001915 ( Main/Corpus ); précédent : 001914; suivant : 001916Mifepristone and spironolactone differently alter cocaine intravenous self-administration and cocaine-induced locomotion in C57BL/6J mice.
Auteurs : Jean-François Fiancette ; Eric Balado ; Pier-Vincenzo Piazza ; Véronique Deroche-GamonetSource :
- Addiction biology [ 1369-1600 ] ; 2010.
English descriptors
- KwdEn :
- Animals (MeSH), Cocaine (toxicity), Cocaine-Related Disorders (psychology), Diuretics (pharmacology), Hallucinogens (toxicity), Hormone Antagonists (pharmacology), Injections, Intraperitoneal (MeSH), Mice (MeSH), Mice, Inbred C57BL (MeSH), Mifepristone (pharmacology), Mineralocorticoid Receptor Antagonists (pharmacology), Motivation (MeSH), Motor Activity (drug effects), Receptors, Glucocorticoid (antagonists & inhibitors), Self Administration (MeSH), Spironolactone (pharmacology), Substance Abuse, Intravenous (psychology).
- MESH :
- chemical , antagonists & inhibitors : Receptors, Glucocorticoid.
- chemical , pharmacology : Diuretics, Hormone Antagonists, Mifepristone, Mineralocorticoid Receptor Antagonists, Spironolactone.
- chemical , toxicity : Cocaine, Hallucinogens.
- drug effects : Motor Activity.
- psychology : Cocaine-Related Disorders, Substance Abuse, Intravenous.
- Animals, Injections, Intraperitoneal, Mice, Mice, Inbred C57BL, Motivation, Self Administration.
Abstract
Corticosterone, the main glucorticoid hormone in rodents, facilitates behavioral responses to cocaine. Corticosterone is proposed to modulate cocaine intravenous self-administration (SA) and cocaine-induced locomotion through distinct receptors, the glucocorticoid receptor (GR) and the mineralocorticoid receptor (MR), respectively. However, this remains debatable. On one hand, modulation of both responses by the GR was tested in different experimental conditions, i.e. light versus dark nycthemeral phase and naïve versus cocaine-experienced animals. On the other hand, modulation of both responses by the MR was never tested directly but only inferred based on the ability of low plasma corticosterone levels (those for which corticosterone almost exclusively binds the MR) to compensate the effects of adrenalectomy. Our goal here was to test the involvement of the GR and the MR in cocaine-induced locomotor and reinforcing effects in the same experimental conditions. C57Bl/6J mice were trained for cocaine (1 mg/kg/infusion) intravenous SA over 40 SA sessions. The animals were then administered with mifepristone (30 mg/kg i.p.), a GR antagonist, or with spironolactone (20 mg/kg/i.p.), an MR antagonist, 2 hours before either cocaine intravenous SA or cocaine-induced locomotion. In a comparable nycthemeral period and in similarly cocaine-experienced animals, a blockade of the GR decreased cocaine-induced reinforcing effects but not cocaine-induced locomotion. A blockade of the MR decreased both cocaine-induced reinforcing (but to a much lesser extent than the GR blockade) and locomotor effects. Altogether, our results comforted the hypothesis that the GR modulates cocaine-related operant conditioning, while the MR would modulate cocaine-related unconditioned effects. The present data also reveal mifepristone as an interesting tool for manipulating the impact of corticosterone on cocaine-induced reinforcing effects in mice.
DOI: 10.1111/j.1369-1600.2009.00178.x
PubMed: 19799583
Links to Exploration step
pubmed:19799583Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Mifepristone and spironolactone differently alter cocaine intravenous self-administration and cocaine-induced locomotion in C57BL/6J mice.</title><author><name sortKey="Fiancette, Jean Francois" sort="Fiancette, Jean Francois" uniqKey="Fiancette J" first="Jean-François" last="Fiancette">Jean-François Fiancette</name><affiliation><nlm:affiliation>INSERM U862, NeuroCentre Magendie, 146 rue Léo Saignat, Bordeaux Cedex, France.</nlm:affiliation></affiliation></author><author><name sortKey="Balado, Eric" sort="Balado, Eric" uniqKey="Balado E" first="Eric" last="Balado">Eric Balado</name></author><author><name sortKey="Piazza, Pier Vincenzo" sort="Piazza, Pier Vincenzo" uniqKey="Piazza P" first="Pier-Vincenzo" last="Piazza">Pier-Vincenzo Piazza</name></author><author><name sortKey="Deroche Gamonet, Veronique" sort="Deroche Gamonet, Veronique" uniqKey="Deroche Gamonet V" first="Véronique" last="Deroche-Gamonet">Véronique Deroche-Gamonet</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2010">2010</date><idno type="RBID">pubmed:19799583</idno><idno type="pmid">19799583</idno><idno type="doi">10.1111/j.1369-1600.2009.00178.x</idno><idno type="wicri:Area/Main/Corpus">001915</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">001915</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Mifepristone and spironolactone differently alter cocaine intravenous self-administration and cocaine-induced locomotion in C57BL/6J mice.</title><author><name sortKey="Fiancette, Jean Francois" sort="Fiancette, Jean Francois" uniqKey="Fiancette J" first="Jean-François" last="Fiancette">Jean-François Fiancette</name><affiliation><nlm:affiliation>INSERM U862, NeuroCentre Magendie, 146 rue Léo Saignat, Bordeaux Cedex, France.</nlm:affiliation></affiliation></author><author><name sortKey="Balado, Eric" sort="Balado, Eric" uniqKey="Balado E" first="Eric" last="Balado">Eric Balado</name></author><author><name sortKey="Piazza, Pier Vincenzo" sort="Piazza, Pier Vincenzo" uniqKey="Piazza P" first="Pier-Vincenzo" last="Piazza">Pier-Vincenzo Piazza</name></author><author><name sortKey="Deroche Gamonet, Veronique" sort="Deroche Gamonet, Veronique" uniqKey="Deroche Gamonet V" first="Véronique" last="Deroche-Gamonet">Véronique Deroche-Gamonet</name></author></analytic><series><title level="j">Addiction biology</title><idno type="eISSN">1369-1600</idno><imprint><date when="2010" type="published">2010</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term><term>Cocaine (toxicity)</term><term>Cocaine-Related Disorders (psychology)</term><term>Diuretics (pharmacology)</term><term>Hallucinogens (toxicity)</term><term>Hormone Antagonists (pharmacology)</term><term>Injections, Intraperitoneal (MeSH)</term><term>Mice (MeSH)</term><term>Mice, Inbred C57BL (MeSH)</term><term>Mifepristone (pharmacology)</term><term>Mineralocorticoid Receptor Antagonists (pharmacology)</term><term>Motivation (MeSH)</term><term>Motor Activity (drug effects)</term><term>Receptors, Glucocorticoid (antagonists & inhibitors)</term><term>Self Administration (MeSH)</term><term>Spironolactone (pharmacology)</term><term>Substance Abuse, Intravenous (psychology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Receptors, Glucocorticoid</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Diuretics</term><term>Hormone Antagonists</term><term>Mifepristone</term><term>Mineralocorticoid Receptor Antagonists</term><term>Spironolactone</term></keywords><keywords scheme="MESH" type="chemical" qualifier="toxicity" xml:lang="en"><term>Cocaine</term><term>Hallucinogens</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Motor Activity</term></keywords><keywords scheme="MESH" qualifier="psychology" xml:lang="en"><term>Cocaine-Related Disorders</term><term>Substance Abuse, Intravenous</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Injections, Intraperitoneal</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Motivation</term><term>Self Administration</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Corticosterone, the main glucorticoid hormone in rodents, facilitates behavioral responses to cocaine. Corticosterone is proposed to modulate cocaine intravenous self-administration (SA) and cocaine-induced locomotion through distinct receptors, the glucocorticoid receptor (GR) and the mineralocorticoid receptor (MR), respectively. However, this remains debatable. On one hand, modulation of both responses by the GR was tested in different experimental conditions, i.e. light versus dark nycthemeral phase and naïve versus cocaine-experienced animals. On the other hand, modulation of both responses by the MR was never tested directly but only inferred based on the ability of low plasma corticosterone levels (those for which corticosterone almost exclusively binds the MR) to compensate the effects of adrenalectomy. Our goal here was to test the involvement of the GR and the MR in cocaine-induced locomotor and reinforcing effects in the same experimental conditions. C57Bl/6J mice were trained for cocaine (1 mg/kg/infusion) intravenous SA over 40 SA sessions. The animals were then administered with mifepristone (30 mg/kg i.p.), a GR antagonist, or with spironolactone (20 mg/kg/i.p.), an MR antagonist, 2 hours before either cocaine intravenous SA or cocaine-induced locomotion. In a comparable nycthemeral period and in similarly cocaine-experienced animals, a blockade of the GR decreased cocaine-induced reinforcing effects but not cocaine-induced locomotion. A blockade of the MR decreased both cocaine-induced reinforcing (but to a much lesser extent than the GR blockade) and locomotor effects. Altogether, our results comforted the hypothesis that the GR modulates cocaine-related operant conditioning, while the MR would modulate cocaine-related unconditioned effects. The present data also reveal mifepristone as an interesting tool for manipulating the impact of corticosterone on cocaine-induced reinforcing effects in mice.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">19799583</PMID><DateCompleted><Year>2010</Year><Month>03</Month><Day>15</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1369-1600</ISSN><JournalIssue CitedMedium="Internet"><Volume>15</Volume><Issue>1</Issue><PubDate><Year>2010</Year><Month>Jan</Month></PubDate></JournalIssue><Title>Addiction biology</Title><ISOAbbreviation>Addict Biol</ISOAbbreviation></Journal><ArticleTitle>Mifepristone and spironolactone differently alter cocaine intravenous self-administration and cocaine-induced locomotion in C57BL/6J mice.</ArticleTitle><Pagination><MedlinePgn>81-7</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1111/j.1369-1600.2009.00178.x</ELocationID><Abstract><AbstractText>Corticosterone, the main glucorticoid hormone in rodents, facilitates behavioral responses to cocaine. Corticosterone is proposed to modulate cocaine intravenous self-administration (SA) and cocaine-induced locomotion through distinct receptors, the glucocorticoid receptor (GR) and the mineralocorticoid receptor (MR), respectively. However, this remains debatable. On one hand, modulation of both responses by the GR was tested in different experimental conditions, i.e. light versus dark nycthemeral phase and naïve versus cocaine-experienced animals. On the other hand, modulation of both responses by the MR was never tested directly but only inferred based on the ability of low plasma corticosterone levels (those for which corticosterone almost exclusively binds the MR) to compensate the effects of adrenalectomy. Our goal here was to test the involvement of the GR and the MR in cocaine-induced locomotor and reinforcing effects in the same experimental conditions. C57Bl/6J mice were trained for cocaine (1 mg/kg/infusion) intravenous SA over 40 SA sessions. The animals were then administered with mifepristone (30 mg/kg i.p.), a GR antagonist, or with spironolactone (20 mg/kg/i.p.), an MR antagonist, 2 hours before either cocaine intravenous SA or cocaine-induced locomotion. In a comparable nycthemeral period and in similarly cocaine-experienced animals, a blockade of the GR decreased cocaine-induced reinforcing effects but not cocaine-induced locomotion. A blockade of the MR decreased both cocaine-induced reinforcing (but to a much lesser extent than the GR blockade) and locomotor effects. Altogether, our results comforted the hypothesis that the GR modulates cocaine-related operant conditioning, while the MR would modulate cocaine-related unconditioned effects. The present data also reveal mifepristone as an interesting tool for manipulating the impact of corticosterone on cocaine-induced reinforcing effects in mice.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Fiancette</LastName><ForeName>Jean-François</ForeName><Initials>JF</Initials><AffiliationInfo><Affiliation>INSERM U862, NeuroCentre Magendie, 146 rue Léo Saignat, Bordeaux Cedex, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Balado</LastName><ForeName>Eric</ForeName><Initials>E</Initials></Author><Author ValidYN="Y"><LastName>Piazza</LastName><ForeName>Pier-Vincenzo</ForeName><Initials>PV</Initials></Author><Author ValidYN="Y"><LastName>Deroche-Gamonet</LastName><ForeName>Véronique</ForeName><Initials>V</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. 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UI="D013148">Spironolactone</NameOfSubstance></Chemical><Chemical><RegistryNumber>320T6RNW1F</RegistryNumber><NameOfSubstance UI="D015735">Mifepristone</NameOfSubstance></Chemical><Chemical><RegistryNumber>I5Y540LHVR</RegistryNumber><NameOfSubstance UI="D003042">Cocaine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003042" MajorTopicYN="N">Cocaine</DescriptorName><QualifierName UI="Q000633" MajorTopicYN="Y">toxicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019970" MajorTopicYN="N">Cocaine-Related Disorders</DescriptorName><QualifierName UI="Q000523" MajorTopicYN="Y">psychology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004232" MajorTopicYN="N">Diuretics</DescriptorName><QualifierName UI="Q000494" 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