Chronic Treatment with the IDO1 Inhibitor 1-Methyl-D-Tryptophan Minimizes the Behavioural and Biochemical Abnormalities Induced by Unpredictable Chronic Mild Stress in Mice - Comparison with Fluoxetine.
Identifieur interne : 001650 ( PubMed/Corpus ); précédent : 001649; suivant : 001651Chronic Treatment with the IDO1 Inhibitor 1-Methyl-D-Tryptophan Minimizes the Behavioural and Biochemical Abnormalities Induced by Unpredictable Chronic Mild Stress in Mice - Comparison with Fluoxetine.
Auteurs : Anthony Laugeray ; Jean-Marie Launay ; Jacques Callebert ; Oguz Mutlu ; Gilles J. Guillemin ; Catherine Belzung ; Pascal R. BaroneSource :
- PloS one [ 1932-6203 ] ; 2016.
English descriptors
- KwdEn :
- Animals, Antidepressive Agents, Second-Generation (pharmacology), Chronic Disease, Cytokines (metabolism), Depression (physiopathology), Depression (prevention & control), Fluoxetine (pharmacology), Indoleamine-Pyrrole 2,3,-Dioxygenase (antagonists & inhibitors), Indoleamine-Pyrrole 2,3,-Dioxygenase (metabolism), Inflammation Mediators (metabolism), Kynurenine (metabolism), Male, Mice, Inbred BALB C, Signal Transduction (drug effects), Stress, Psychological (physiopathology), Stress, Psychological (prevention & control), Time Factors, Tryptophan (analogs & derivatives), Tryptophan (pharmacology).
- MESH :
- chemical , analogs & derivatives : Tryptophan.
- chemical , antagonists & inhibitors : Indoleamine-Pyrrole 2,3,-Dioxygenase.
- chemical , metabolism : Cytokines, Indoleamine-Pyrrole 2,3,-Dioxygenase, Inflammation Mediators, Kynurenine.
- chemical , pharmacology : Antidepressive Agents, Second-Generation, Fluoxetine, Tryptophan.
- drug effects : Signal Transduction.
- physiopathology : Depression, Stress, Psychological.
- prevention & control : Depression, Stress, Psychological.
- Animals, Chronic Disease, Male, Mice, Inbred BALB C, Time Factors.
Abstract
We demonstrated that confronting mice to the Unpredictable Chronic Mild Stress (UCMS) procedure-a validated model of stress-induced depression-results in behavioural alterations and biochemical changes in the kynurenine pathway (KP), suspected to modify the glutamatergic neurotransmission through the imbalance between downstream metabolites such as 3-hydroxykynurenine, quinolinic and kynurenic acids. We showed that daily treatment with the IDO1 inhibitor 1-methyl-D-tryptophan partially rescues UCMS-induced KP alterations as does the antidepressant fluoxetine. More importantly we demonstrated that 1-methyl-D-tryptophan was able to alleviate most of the behavioural changes resulting from UCMS exposure. We also showed that both fluoxetine and 1-methyl-D-tryptophan robustly reduced peripheral levels of proinflammatory cytokines in UCMS mice suggesting that their therapeutic effects might occur through anti-inflammatory processes. KP inhibition might be involved in the positive effects of fluoxetine on mice behaviour and could be a relevant strategy to counteract depressive-like symptoms.
DOI: 10.1371/journal.pone.0164337
PubMed: 27828964
Links to Exploration step
pubmed:27828964Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Chronic Treatment with the IDO1 Inhibitor 1-Methyl-D-Tryptophan Minimizes the Behavioural and Biochemical Abnormalities Induced by Unpredictable Chronic Mild Stress in Mice - Comparison with Fluoxetine.</title><author><name sortKey="Laugeray, Anthony" sort="Laugeray, Anthony" uniqKey="Laugeray A" first="Anthony" last="Laugeray">Anthony Laugeray</name><affiliation><nlm:affiliation>Molecular and Experimental Immunology and Neurogenetics - UMR7355, CNRS - 3b Rue de Férollerie, Orléans La Source, Cedex 2, France.</nlm:affiliation></affiliation></author><author><name sortKey="Launay, Jean Marie" sort="Launay, Jean Marie" uniqKey="Launay J" first="Jean-Marie" last="Launay">Jean-Marie Launay</name><affiliation><nlm:affiliation>UMRS INSERM U942, Service de Biochimie, Hôpital Lariboisière, Assistance Publique - Hôpitaux de Paris, Paris, France.</nlm:affiliation></affiliation></author><author><name sortKey="Callebert, Jacques" sort="Callebert, Jacques" uniqKey="Callebert J" first="Jacques" last="Callebert">Jacques Callebert</name><affiliation><nlm:affiliation>UMRS INSERM U942, Service de Biochimie, Hôpital Lariboisière, Assistance Publique - Hôpitaux de Paris, Paris, France.</nlm:affiliation></affiliation></author><author><name sortKey="Mutlu, Oguz" sort="Mutlu, Oguz" uniqKey="Mutlu O" first="Oguz" last="Mutlu">Oguz Mutlu</name><affiliation><nlm:affiliation>UMRS INSERM U930, CNRS ERL 3106, Université François Rabelais, Tours, France.</nlm:affiliation></affiliation></author><author><name sortKey="Guillemin, Gilles J" sort="Guillemin, Gilles J" uniqKey="Guillemin G" first="Gilles J" last="Guillemin">Gilles J. Guillemin</name><affiliation><nlm:affiliation>Neuroinflammation Group, Faculty of Medicine and Health Sciences, Macquarie University, NSW, Sydney, Australia.</nlm:affiliation></affiliation></author><author><name sortKey="Belzung, Catherine" sort="Belzung, Catherine" uniqKey="Belzung C" first="Catherine" last="Belzung">Catherine Belzung</name><affiliation><nlm:affiliation>UMRS INSERM U930, CNRS ERL 3106, Université François Rabelais, Tours, France.</nlm:affiliation></affiliation></author><author><name sortKey="Barone, Pascal R" sort="Barone, Pascal R" uniqKey="Barone P" first="Pascal R" last="Barone">Pascal R. Barone</name><affiliation><nlm:affiliation>UMRS INSERM U930, CNRS ERL 3106, Université François Rabelais, Tours, France.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2016">2016</date><idno type="RBID">pubmed:27828964</idno><idno type="pmid">27828964</idno><idno type="doi">10.1371/journal.pone.0164337</idno><idno type="wicri:Area/PubMed/Corpus">001650</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001650</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Chronic Treatment with the IDO1 Inhibitor 1-Methyl-D-Tryptophan Minimizes the Behavioural and Biochemical Abnormalities Induced by Unpredictable Chronic Mild Stress in Mice - Comparison with Fluoxetine.</title><author><name sortKey="Laugeray, Anthony" sort="Laugeray, Anthony" uniqKey="Laugeray A" first="Anthony" last="Laugeray">Anthony Laugeray</name><affiliation><nlm:affiliation>Molecular and Experimental Immunology and Neurogenetics - UMR7355, CNRS - 3b Rue de Férollerie, Orléans La Source, Cedex 2, France.</nlm:affiliation></affiliation></author><author><name sortKey="Launay, Jean Marie" sort="Launay, Jean Marie" uniqKey="Launay J" first="Jean-Marie" last="Launay">Jean-Marie Launay</name><affiliation><nlm:affiliation>UMRS INSERM U942, Service de Biochimie, Hôpital Lariboisière, Assistance Publique - Hôpitaux de Paris, Paris, France.</nlm:affiliation></affiliation></author><author><name sortKey="Callebert, Jacques" sort="Callebert, Jacques" uniqKey="Callebert J" first="Jacques" last="Callebert">Jacques Callebert</name><affiliation><nlm:affiliation>UMRS INSERM U942, Service de Biochimie, Hôpital Lariboisière, Assistance Publique - Hôpitaux de Paris, Paris, France.</nlm:affiliation></affiliation></author><author><name sortKey="Mutlu, Oguz" sort="Mutlu, Oguz" uniqKey="Mutlu O" first="Oguz" last="Mutlu">Oguz Mutlu</name><affiliation><nlm:affiliation>UMRS INSERM U930, CNRS ERL 3106, Université François Rabelais, Tours, France.</nlm:affiliation></affiliation></author><author><name sortKey="Guillemin, Gilles J" sort="Guillemin, Gilles J" uniqKey="Guillemin G" first="Gilles J" last="Guillemin">Gilles J. Guillemin</name><affiliation><nlm:affiliation>Neuroinflammation Group, Faculty of Medicine and Health Sciences, Macquarie University, NSW, Sydney, Australia.</nlm:affiliation></affiliation></author><author><name sortKey="Belzung, Catherine" sort="Belzung, Catherine" uniqKey="Belzung C" first="Catherine" last="Belzung">Catherine Belzung</name><affiliation><nlm:affiliation>UMRS INSERM U930, CNRS ERL 3106, Université François Rabelais, Tours, France.</nlm:affiliation></affiliation></author><author><name sortKey="Barone, Pascal R" sort="Barone, Pascal R" uniqKey="Barone P" first="Pascal R" last="Barone">Pascal R. Barone</name><affiliation><nlm:affiliation>UMRS INSERM U930, CNRS ERL 3106, Université François Rabelais, Tours, France.</nlm:affiliation></affiliation></author></analytic><series><title level="j">PloS one</title><idno type="eISSN">1932-6203</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Antidepressive Agents, Second-Generation (pharmacology)</term><term>Chronic Disease</term><term>Cytokines (metabolism)</term><term>Depression (physiopathology)</term><term>Depression (prevention & control)</term><term>Fluoxetine (pharmacology)</term><term>Indoleamine-Pyrrole 2,3,-Dioxygenase (antagonists & inhibitors)</term><term>Indoleamine-Pyrrole 2,3,-Dioxygenase (metabolism)</term><term>Inflammation Mediators (metabolism)</term><term>Kynurenine (metabolism)</term><term>Male</term><term>Mice, Inbred BALB C</term><term>Signal Transduction (drug effects)</term><term>Stress, Psychological (physiopathology)</term><term>Stress, Psychological (prevention & control)</term><term>Time Factors</term><term>Tryptophan (analogs & derivatives)</term><term>Tryptophan (pharmacology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Tryptophan</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Indoleamine-Pyrrole 2,3,-Dioxygenase</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Cytokines</term><term>Indoleamine-Pyrrole 2,3,-Dioxygenase</term><term>Inflammation Mediators</term><term>Kynurenine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antidepressive Agents, Second-Generation</term><term>Fluoxetine</term><term>Tryptophan</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Signal Transduction</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Depression</term><term>Stress, Psychological</term></keywords><keywords scheme="MESH" qualifier="prevention & control" xml:lang="en"><term>Depression</term><term>Stress, Psychological</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Chronic Disease</term><term>Male</term><term>Mice, Inbred BALB C</term><term>Time Factors</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We demonstrated that confronting mice to the Unpredictable Chronic Mild Stress (UCMS) procedure-a validated model of stress-induced depression-results in behavioural alterations and biochemical changes in the kynurenine pathway (KP), suspected to modify the glutamatergic neurotransmission through the imbalance between downstream metabolites such as 3-hydroxykynurenine, quinolinic and kynurenic acids. We showed that daily treatment with the IDO1 inhibitor 1-methyl-D-tryptophan partially rescues UCMS-induced KP alterations as does the antidepressant fluoxetine. More importantly we demonstrated that 1-methyl-D-tryptophan was able to alleviate most of the behavioural changes resulting from UCMS exposure. We also showed that both fluoxetine and 1-methyl-D-tryptophan robustly reduced peripheral levels of proinflammatory cytokines in UCMS mice suggesting that their therapeutic effects might occur through anti-inflammatory processes. KP inhibition might be involved in the positive effects of fluoxetine on mice behaviour and could be a relevant strategy to counteract depressive-like symptoms.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">27828964</PMID><DateCreated><Year>2016</Year><Month>11</Month><Day>09</Day></DateCreated><DateCompleted><Year>2017</Year><Month>07</Month><Day>03</Day></DateCompleted><DateRevised><Year>2017</Year><Month>07</Month><Day>03</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Electronic">1932-6203</ISSN><JournalIssue CitedMedium="Internet"><Volume>11</Volume><Issue>11</Issue><PubDate><Year>2016</Year></PubDate></JournalIssue><Title>PloS one</Title><ISOAbbreviation>PLoS ONE</ISOAbbreviation></Journal><ArticleTitle>Chronic Treatment with the IDO1 Inhibitor 1-Methyl-D-Tryptophan Minimizes the Behavioural and Biochemical Abnormalities Induced by Unpredictable Chronic Mild Stress in Mice - Comparison with Fluoxetine.</ArticleTitle><Pagination><MedlinePgn>e0164337</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1371/journal.pone.0164337</ELocationID><Abstract><AbstractText>We demonstrated that confronting mice to the Unpredictable Chronic Mild Stress (UCMS) procedure-a validated model of stress-induced depression-results in behavioural alterations and biochemical changes in the kynurenine pathway (KP), suspected to modify the glutamatergic neurotransmission through the imbalance between downstream metabolites such as 3-hydroxykynurenine, quinolinic and kynurenic acids. We showed that daily treatment with the IDO1 inhibitor 1-methyl-D-tryptophan partially rescues UCMS-induced KP alterations as does the antidepressant fluoxetine. More importantly we demonstrated that 1-methyl-D-tryptophan was able to alleviate most of the behavioural changes resulting from UCMS exposure. We also showed that both fluoxetine and 1-methyl-D-tryptophan robustly reduced peripheral levels of proinflammatory cytokines in UCMS mice suggesting that their therapeutic effects might occur through anti-inflammatory processes. KP inhibition might be involved in the positive effects of fluoxetine on mice behaviour and could be a relevant strategy to counteract depressive-like symptoms.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Laugeray</LastName><ForeName>Anthony</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Molecular and Experimental Immunology and Neurogenetics - UMR7355, CNRS - 3b Rue de Férollerie, Orléans La Source, Cedex 2, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Launay</LastName><ForeName>Jean-Marie</ForeName><Initials>JM</Initials><AffiliationInfo><Affiliation>UMRS INSERM U942, Service de Biochimie, Hôpital Lariboisière, Assistance Publique - Hôpitaux de Paris, Paris, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Callebert</LastName><ForeName>Jacques</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>UMRS INSERM U942, Service de Biochimie, Hôpital Lariboisière, Assistance Publique - Hôpitaux de Paris, Paris, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mutlu</LastName><ForeName>Oguz</ForeName><Initials>O</Initials><AffiliationInfo><Affiliation>UMRS INSERM U930, CNRS ERL 3106, Université François Rabelais, Tours, France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Pharmacology, Faculty of Medicine, Kocaeli University, 41380 Kocaeli, Turkey.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Guillemin</LastName><ForeName>Gilles J</ForeName><Initials>GJ</Initials><AffiliationInfo><Affiliation>Neuroinflammation Group, Faculty of Medicine and Health Sciences, Macquarie University, NSW, Sydney, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Belzung</LastName><ForeName>Catherine</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>UMRS INSERM U930, CNRS ERL 3106, Université François Rabelais, Tours, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Barone</LastName><ForeName>Pascal R</ForeName><Initials>PR</Initials><AffiliationInfo><Affiliation>UMRS INSERM U930, CNRS ERL 3106, Université François Rabelais, Tours, France.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D003160">Comparative Study</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2016</Year><Month>11</Month><Day>09</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>PLoS One</MedlineTA><NlmUniqueID>101285081</NlmUniqueID><ISSNLinking>1932-6203</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C525396">1-methyltryptophan</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance 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MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007737" MajorTopicYN="N">Kynurenine</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008807" MajorTopicYN="N">Mice, Inbred BALB C</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013315" MajorTopicYN="N">Stress, Psychological</DescriptorName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName><QualifierName UI="Q000517" MajorTopicYN="Y">prevention & control</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013997" MajorTopicYN="N">Time Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014364" MajorTopicYN="N">Tryptophan</DescriptorName><QualifierName UI="Q000031" MajorTopicYN="Y">analogs & derivatives</QualifierName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading></MeshHeadingList><CoiStatement>The authors have declared that no competing interests exist.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2016</Year><Month>05</Month><Day>17</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2016</Year><Month>09</Month><Day>22</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2016</Year><Month>11</Month><Day>10</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2016</Year><Month>11</Month><Day>10</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2017</Year><Month>7</Month><Day>4</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">27828964</ArticleId><ArticleId IdType="doi">10.1371/journal.pone.0164337</ArticleId><ArticleId IdType="pii">PONE-D-16-19885</ArticleId><ArticleId IdType="pmc">PMC5102430</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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