AustralieFrV1, PubMed, Checkpoint, bibRecord, 000D38

Elevated CYP2C19 expression is associated with depressive symptoms and hippocampal homeostasis impairment.

Identifieur interne : 000D38 ( PubMed/Checkpoint ); précédent : 000D37; suivant : 000D39

Elevated CYP2C19 expression is associated with depressive symptoms and hippocampal homeostasis impairment.

Auteurs : M M Juki [Suède] ; N. Opel [Allemagne] ; J. Ström [Suède] ; T. Carrillo-Roa [Allemagne] ; S. Miksys [Canada] ; M. Novalen [Canada] ; A. Renblom [Suède] ; S C Sim [Suède] ; E M Pe As-Lled [Espagne] ; P. Courtet [France] ; A. Llerena [Canada] ; B T Baune [Australie] ; D J De Quervain [Suisse] ; A. Papassotiropoulos [Suisse] ; R F Tyndale [Canada] ; E B Binder [Allemagne] ; U. Dannlowski [Allemagne] ; M. Ingelman-Sundberg [Suède]

Source :

Molecular psychiatry [ 1476-5578 ] ; 2017.

RBID : pubmed:27895323

Descripteurs français

KwdFr :
- Afro-Américains (génétique), Agonistes des récepteurs 5-HT1 de la sérotonine (pharmacologie), Animaux, Anxiété (génétique), Anxiété (imagerie diagnostique), Citalopram (pharmacologie), Comportement animal (), Cytochrome P-450 CYP2C19 (), Cytochrome P-450 CYP2C19 (génétique), Cytochrome P-450 CYP2C19 (métabolisme), Dépression (génétique), Dépression (traitement médicamenteux), Facteur neurotrophique dérivé du cerveau (métabolisme), Hippocampe (métabolisme), Homéostasie (génétique), Homéostasie (physiologie), Humains, Neurogenèse (génétique), Récepteur de la sérotonine de type 5-HT1A (métabolisme), Souris, Souris transgéniques, Sérotonine (métabolisme), Trouble dépressif majeur (imagerie diagnostique), Trouble dépressif majeur (métabolisme), Troubles anxieux (génétique).
MESH :
- génétique : Afro-Américains, Anxiété, Cytochrome P-450 CYP2C19, Dépression, Homéostasie, Neurogenèse, Troubles anxieux.
- imagerie diagnostique : Anxiété, Trouble dépressif majeur.
- métabolisme : Cytochrome P-450 CYP2C19, Facteur neurotrophique dérivé du cerveau, Hippocampe, Récepteur de la sérotonine de type 5-HT1A, Sérotonine, Trouble dépressif majeur.
- pharmacologie : Agonistes des récepteurs 5-HT1 de la sérotonine, Citalopram.
- physiologie : Homéostasie.
- traitement médicamenteux : Dépression.
- Animaux, Comportement animal, Cytochrome P-450 CYP2C19, Humains, Souris, Souris transgéniques.

English descriptors

KwdEn :
- African Americans (genetics), Animals, Anxiety (diagnostic imaging), Anxiety (genetics), Anxiety Disorders (genetics), Behavior, Animal (drug effects), Brain-Derived Neurotrophic Factor (metabolism), Citalopram (pharmacology), Cytochrome P-450 CYP2C19 (drug effects), Cytochrome P-450 CYP2C19 (genetics), Cytochrome P-450 CYP2C19 (metabolism), Depression (drug therapy), Depression (genetics), Depressive Disorder, Major (diagnostic imaging), Depressive Disorder, Major (metabolism), Hippocampus (metabolism), Homeostasis (genetics), Homeostasis (physiology), Humans, Mice, Mice, Transgenic, Neurogenesis (genetics), Receptor, Serotonin, 5-HT1A (metabolism), Serotonin (metabolism), Serotonin 5-HT1 Receptor Agonists (pharmacology).
MESH :
- chemical , drug effects : Cytochrome P-450 CYP2C19.
- chemical , genetics : Cytochrome P-450 CYP2C19.
- chemical , metabolism : Brain-Derived Neurotrophic Factor, Cytochrome P-450 CYP2C19, Receptor, Serotonin, 5-HT1A, Serotonin.
- diagnostic imaging : Anxiety, Depressive Disorder, Major.
- drug effects : Behavior, Animal.
- drug therapy : Depression.
- genetics : African Americans, Anxiety, Anxiety Disorders, Depression, Homeostasis, Neurogenesis.
- metabolism : Depressive Disorder, Major, Hippocampus.
- chemical , pharmacology : Citalopram, Serotonin 5-HT1 Receptor Agonists.
- physiology : Homeostasis.
- Animals, Humans, Mice, Mice, Transgenic.

Abstract

The polymorphic CYP2C19 enzyme metabolizes psychoactive compounds and is expressed in the adult liver and fetal brain. Previously, we demonstrated that the absence of CYP2C19 is associated with lower levels of depressive symptoms in 1472 Swedes. Conversely, transgenic mice carrying the human CYP2C19 gene (2C19TG) have shown an anxious phenotype and decrease in hippocampal volume and adult neurogenesis. The aims of this study were to: (1) examine whether the 2C19TG findings could be translated to humans, (2) evaluate the usefulness of the 2C19TG strain as a tool for preclinical screening of new antidepressants and (3) provide an insight into the molecular underpinnings of the 2C19TG phenotype. In humans, we found that the absence of CYP2C19 was associated with a bilateral hippocampal volume increase in two independent healthy cohorts (N=386 and 1032) and a lower prevalence of major depressive disorder and depression severity in African-Americans (N=3848). Moreover, genetically determined high CYP2C19 enzymatic capacity was associated with higher suicidality in depressed suicide attempters (N=209). 2C19TG mice showed high stress sensitivity, impaired hippocampal Bdnf homeostasis in stress, and more despair-like behavior in the forced swim test (FST). After the treatment with citalopram and 5-HT1A receptor agonist 8OH-DPAT, the reduction in immobility time in the FST was more pronounced in 2C19TG mice compared with WTs. Conversely, in the 2C19TG hippocampus, metabolic turnover of serotonin was reduced, whereas ERK1/2 and GSK3β phosphorylation was increased. Altogether, this study indicates that elevated CYP2C19 expression is associated with depressive symptoms, reduced hippocampal volume and impairment of hippocampal serotonin and BDNF homeostasis.

DOI: 10.1038/mp.2016.204
PubMed: 27895323

Affiliations:

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Le document en format XML

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<author><name sortKey="Pe As Lled, E M" sort="Pe As Lled, E M" uniqKey="Pe As Lled E" first="E M" last="Pe As-Lled">E M Pe As-Lled</name>
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<author><name sortKey="Courtet, P" sort="Courtet, P" uniqKey="Courtet P" first="P" last="Courtet">P. Courtet</name>
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<author><name sortKey="Baune, B T" sort="Baune, B T" uniqKey="Baune B" first="B T" last="Baune">B T Baune</name>
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<author><name sortKey="De Quervain, D J" sort="De Quervain, D J" uniqKey="De Quervain D" first="D J" last="De Quervain">D J De Quervain</name>
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<author><name sortKey="Papassotiropoulos, A" sort="Papassotiropoulos, A" uniqKey="Papassotiropoulos A" first="A" last="Papassotiropoulos">A. Papassotiropoulos</name>
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<author><name sortKey="Dannlowski, U" sort="Dannlowski, U" uniqKey="Dannlowski U" first="U" last="Dannlowski">U. Dannlowski</name>
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<author><name sortKey="Ingelman Sundberg, M" sort="Ingelman Sundberg, M" uniqKey="Ingelman Sundberg M" first="M" last="Ingelman-Sundberg">M. Ingelman-Sundberg</name>
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<country xml:lang="fr">Suède</country>
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<author><name sortKey="Opel, N" sort="Opel, N" uniqKey="Opel N" first="N" last="Opel">N. Opel</name>
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<country xml:lang="fr">Allemagne</country>
<wicri:regionArea>Department of Psychiatry, University of Münster, Münster</wicri:regionArea>
<placeName><region type="land" nuts="1">Rhénanie-du-Nord-Westphalie</region>
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<author><name sortKey="Strom, J" sort="Strom, J" uniqKey="Strom J" first="J" last="Ström">J. Ström</name>
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<country xml:lang="fr">Suède</country>
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<author><name sortKey="Carrillo Roa, T" sort="Carrillo Roa, T" uniqKey="Carrillo Roa T" first="T" last="Carrillo-Roa">T. Carrillo-Roa</name>
<affiliation wicri:level="3"><nlm:affiliation>Department of Translational Research in Psychiatry, Max Planck Institute of Psychiatry, Munich, Germany.</nlm:affiliation>
<country xml:lang="fr">Allemagne</country>
<wicri:regionArea>Department of Translational Research in Psychiatry, Max Planck Institute of Psychiatry, Munich</wicri:regionArea>
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<region type="district" nuts="2">District de Haute-Bavière</region>
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<author><name sortKey="Miksys, S" sort="Miksys, S" uniqKey="Miksys S" first="S" last="Miksys">S. Miksys</name>
<affiliation wicri:level="1"><nlm:affiliation>Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health, Toronto, ON, Canada.</nlm:affiliation>
<country xml:lang="fr">Canada</country>
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<author><name sortKey="Novalen, M" sort="Novalen, M" uniqKey="Novalen M" first="M" last="Novalen">M. Novalen</name>
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<author><name sortKey="Renblom, A" sort="Renblom, A" uniqKey="Renblom A" first="A" last="Renblom">A. Renblom</name>
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<author><name sortKey="Sim, S C" sort="Sim, S C" uniqKey="Sim S" first="S C" last="Sim">S C Sim</name>
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<country xml:lang="fr">Suède</country>
<wicri:regionArea>Section of Pharmacogenetics, Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm</wicri:regionArea>
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<author><name sortKey="Pe As Lled, E M" sort="Pe As Lled, E M" uniqKey="Pe As Lled E" first="E M" last="Pe As-Lled">E M Pe As-Lled</name>
<affiliation wicri:level="1"><nlm:affiliation>CICAB Clinical Research Center, Extremadura University Hospital and Medical School, Badajoz, Spain.</nlm:affiliation>
<country xml:lang="fr">Espagne</country>
<wicri:regionArea>CICAB Clinical Research Center, Extremadura University Hospital and Medical School, Badajoz</wicri:regionArea>
<wicri:noRegion>Badajoz</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Courtet, P" sort="Courtet, P" uniqKey="Courtet P" first="P" last="Courtet">P. Courtet</name>
<affiliation wicri:level="3"><nlm:affiliation>CHU Montpellier, Hôpital Lapeyronie, Psychiatric Emergency and Post-Acute Care Department, Pole Urgence, Montpellier, France.</nlm:affiliation>
<country xml:lang="fr">France</country>
<wicri:regionArea>CHU Montpellier, Hôpital Lapeyronie, Psychiatric Emergency and Post-Acute Care Department, Pole Urgence, Montpellier</wicri:regionArea>
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<author><name sortKey="Llerena, A" sort="Llerena, A" uniqKey="Llerena A" first="A" last="Llerena">A. Llerena</name>
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<country xml:lang="fr">Canada</country>
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<wicri:noRegion>ON</wicri:noRegion>
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<author><name sortKey="Baune, B T" sort="Baune, B T" uniqKey="Baune B" first="B T" last="Baune">B T Baune</name>
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<country xml:lang="fr">Australie</country>
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<wicri:noRegion>SA</wicri:noRegion>
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<author><name sortKey="De Quervain, D J" sort="De Quervain, D J" uniqKey="De Quervain D" first="D J" last="De Quervain">D J De Quervain</name>
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<region type="district" nuts="2">District de Münster</region>
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<author><name sortKey="Ingelman Sundberg, M" sort="Ingelman Sundberg, M" uniqKey="Ingelman Sundberg M" first="M" last="Ingelman-Sundberg">M. Ingelman-Sundberg</name>
<affiliation wicri:level="3"><nlm:affiliation>Section of Pharmacogenetics, Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.</nlm:affiliation>
<country xml:lang="fr">Suède</country>
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<series><title level="j">Molecular psychiatry</title>
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<term>Animals</term>
<term>Anxiety (diagnostic imaging)</term>
<term>Anxiety (genetics)</term>
<term>Anxiety Disorders (genetics)</term>
<term>Behavior, Animal (drug effects)</term>
<term>Brain-Derived Neurotrophic Factor (metabolism)</term>
<term>Citalopram (pharmacology)</term>
<term>Cytochrome P-450 CYP2C19 (drug effects)</term>
<term>Cytochrome P-450 CYP2C19 (genetics)</term>
<term>Cytochrome P-450 CYP2C19 (metabolism)</term>
<term>Depression (drug therapy)</term>
<term>Depression (genetics)</term>
<term>Depressive Disorder, Major (diagnostic imaging)</term>
<term>Depressive Disorder, Major (metabolism)</term>
<term>Hippocampus (metabolism)</term>
<term>Homeostasis (genetics)</term>
<term>Homeostasis (physiology)</term>
<term>Humans</term>
<term>Mice</term>
<term>Mice, Transgenic</term>
<term>Neurogenesis (genetics)</term>
<term>Receptor, Serotonin, 5-HT1A (metabolism)</term>
<term>Serotonin (metabolism)</term>
<term>Serotonin 5-HT1 Receptor Agonists (pharmacology)</term>
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<term>Agonistes des récepteurs 5-HT1 de la sérotonine (pharmacologie)</term>
<term>Animaux</term>
<term>Anxiété (génétique)</term>
<term>Anxiété (imagerie diagnostique)</term>
<term>Citalopram (pharmacologie)</term>
<term>Comportement animal ()</term>
<term>Cytochrome P-450 CYP2C19 ()</term>
<term>Cytochrome P-450 CYP2C19 (génétique)</term>
<term>Cytochrome P-450 CYP2C19 (métabolisme)</term>
<term>Dépression (génétique)</term>
<term>Dépression (traitement médicamenteux)</term>
<term>Facteur neurotrophique dérivé du cerveau (métabolisme)</term>
<term>Hippocampe (métabolisme)</term>
<term>Homéostasie (génétique)</term>
<term>Homéostasie (physiologie)</term>
<term>Humains</term>
<term>Neurogenèse (génétique)</term>
<term>Récepteur de la sérotonine de type 5-HT1A (métabolisme)</term>
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<term>Souris transgéniques</term>
<term>Sérotonine (métabolisme)</term>
<term>Trouble dépressif majeur (imagerie diagnostique)</term>
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<term>Hippocampus</term>
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<term>Facteur neurotrophique dérivé du cerveau</term>
<term>Hippocampe</term>
<term>Récepteur de la sérotonine de type 5-HT1A</term>
<term>Sérotonine</term>
<term>Trouble dépressif majeur</term>
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<term>Citalopram</term>
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<term>Comportement animal</term>
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<front><div type="abstract" xml:lang="en">The polymorphic CYP2C19 enzyme metabolizes psychoactive compounds and is expressed in the adult liver and fetal brain. Previously, we demonstrated that the absence of CYP2C19 is associated with lower levels of depressive symptoms in 1472 Swedes. Conversely, transgenic mice carrying the human CYP2C19 gene (2C19TG) have shown an anxious phenotype and decrease in hippocampal volume and adult neurogenesis. The aims of this study were to: (1) examine whether the 2C19TG findings could be translated to humans, (2) evaluate the usefulness of the 2C19TG strain as a tool for preclinical screening of new antidepressants and (3) provide an insight into the molecular underpinnings of the 2C19TG phenotype. In humans, we found that the absence of CYP2C19 was associated with a bilateral hippocampal volume increase in two independent healthy cohorts (N=386 and 1032) and a lower prevalence of major depressive disorder and depression severity in African-Americans (N=3848). Moreover, genetically determined high CYP2C19 enzymatic capacity was associated with higher suicidality in depressed suicide attempters (N=209). 2C19TG mice showed high stress sensitivity, impaired hippocampal Bdnf homeostasis in stress, and more despair-like behavior in the forced swim test (FST). After the treatment with citalopram and 5-HT1A receptor agonist 8OH-DPAT, the reduction in immobility time in the FST was more pronounced in 2C19TG mice compared with WTs. Conversely, in the 2C19TG hippocampus, metabolic turnover of serotonin was reduced, whereas ERK1/2 and GSK3β phosphorylation was increased. Altogether, this study indicates that elevated CYP2C19 expression is associated with depressive symptoms, reduced hippocampal volume and impairment of hippocampal serotonin and BDNF homeostasis.</div>
</front>
</TEI>
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<DateCreated><Year>2016</Year>
<Month>11</Month>
<Day>29</Day>
</DateCreated>
<DateCompleted><Year>2017</Year>
<Month>11</Month>
<Day>13</Day>
</DateCompleted>
<DateRevised><Year>2017</Year>
<Month>11</Month>
<Day>13</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1476-5578</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>22</Volume>
<Issue>8</Issue>
<PubDate><Year>2017</Year>
<Month>Aug</Month>
</PubDate>
</JournalIssue>
<Title>Molecular psychiatry</Title>
<ISOAbbreviation>Mol. Psychiatry</ISOAbbreviation>
</Journal>
<ArticleTitle>Elevated CYP2C19 expression is associated with depressive symptoms and hippocampal homeostasis impairment.</ArticleTitle>
<Pagination><MedlinePgn>1155-1163</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1038/mp.2016.204</ELocationID>
<Abstract><AbstractText>The polymorphic CYP2C19 enzyme metabolizes psychoactive compounds and is expressed in the adult liver and fetal brain. Previously, we demonstrated that the absence of CYP2C19 is associated with lower levels of depressive symptoms in 1472 Swedes. Conversely, transgenic mice carrying the human CYP2C19 gene (2C19TG) have shown an anxious phenotype and decrease in hippocampal volume and adult neurogenesis. The aims of this study were to: (1) examine whether the 2C19TG findings could be translated to humans, (2) evaluate the usefulness of the 2C19TG strain as a tool for preclinical screening of new antidepressants and (3) provide an insight into the molecular underpinnings of the 2C19TG phenotype. In humans, we found that the absence of CYP2C19 was associated with a bilateral hippocampal volume increase in two independent healthy cohorts (N=386 and 1032) and a lower prevalence of major depressive disorder and depression severity in African-Americans (N=3848). Moreover, genetically determined high CYP2C19 enzymatic capacity was associated with higher suicidality in depressed suicide attempters (N=209). 2C19TG mice showed high stress sensitivity, impaired hippocampal Bdnf homeostasis in stress, and more despair-like behavior in the forced swim test (FST). After the treatment with citalopram and 5-HT1A receptor agonist 8OH-DPAT, the reduction in immobility time in the FST was more pronounced in 2C19TG mice compared with WTs. Conversely, in the 2C19TG hippocampus, metabolic turnover of serotonin was reduced, whereas ERK1/2 and GSK3β phosphorylation was increased. Altogether, this study indicates that elevated CYP2C19 expression is associated with depressive symptoms, reduced hippocampal volume and impairment of hippocampal serotonin and BDNF homeostasis.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Jukić</LastName>
<ForeName>M M</ForeName>
<Initials>MM</Initials>
<AffiliationInfo><Affiliation>Section of Pharmacogenetics, Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Opel</LastName>
<ForeName>N</ForeName>
<Initials>N</Initials>
<AffiliationInfo><Affiliation>Department of Psychiatry, University of Münster, Münster, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Ström</LastName>
<ForeName>J</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Section of Pharmacogenetics, Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Carrillo-Roa</LastName>
<ForeName>T</ForeName>
<Initials>T</Initials>
<AffiliationInfo><Affiliation>Department of Translational Research in Psychiatry, Max Planck Institute of Psychiatry, Munich, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Miksys</LastName>
<ForeName>S</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health, Toronto, ON, Canada.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Psychiatry, University of Toronto, Toronto, ON, Canada.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Pharmacology and Toxicology, University of Toronto, Toronto, ON, Canada.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Novalen</LastName>
<ForeName>M</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health, Toronto, ON, Canada.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Psychiatry, University of Toronto, Toronto, ON, Canada.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Pharmacology and Toxicology, University of Toronto, Toronto, ON, Canada.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Renblom</LastName>
<ForeName>A</ForeName>
<Initials>A</Initials>
<AffiliationInfo><Affiliation>Section of Pharmacogenetics, Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Sim</LastName>
<ForeName>S C</ForeName>
<Initials>SC</Initials>
<AffiliationInfo><Affiliation>Section of Pharmacogenetics, Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Peñas-Lledó</LastName>
<ForeName>E M</ForeName>
<Initials>EM</Initials>
<AffiliationInfo><Affiliation>CICAB Clinical Research Center, Extremadura University Hospital and Medical School, Badajoz, Spain.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>CIBERSAM, Madrid, Spain.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Courtet</LastName>
<ForeName>P</ForeName>
<Initials>P</Initials>
<AffiliationInfo><Affiliation>CHU Montpellier, Hôpital Lapeyronie, Psychiatric Emergency and Post-Acute Care Department, Pole Urgence, Montpellier, France.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Llerena</LastName>
<ForeName>A</ForeName>
<Initials>A</Initials>
<AffiliationInfo><Affiliation>Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health, Toronto, ON, Canada.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Psychiatry, University of Toronto, Toronto, ON, Canada.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Pharmacology and Toxicology, University of Toronto, Toronto, ON, Canada.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Baune</LastName>
<ForeName>B T</ForeName>
<Initials>BT</Initials>
<AffiliationInfo><Affiliation>Discipline of Psychiatry, School of Medicine, University of Adelaide, Adelaide, SA, Australia.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>de Quervain</LastName>
<ForeName>D J</ForeName>
<Initials>DJ</Initials>
<AffiliationInfo><Affiliation>Transfaculty Research Platform, Department of Psychology, University Psychiatric Clinics, University of Basel, Basel, Switzerland.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Papassotiropoulos</LastName>
<ForeName>A</ForeName>
<Initials>A</Initials>
<AffiliationInfo><Affiliation>Transfaculty Research Platform, Department of Psychology, University Psychiatric Clinics, University of Basel, Basel, Switzerland.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Life Sciences Training Facility, Department Biozentrum, University of Basel, Basel, Switzerland.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Tyndale</LastName>
<ForeName>R F</ForeName>
<Initials>RF</Initials>
<AffiliationInfo><Affiliation>Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health, Toronto, ON, Canada.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Psychiatry, University of Toronto, Toronto, ON, Canada.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Pharmacology and Toxicology, University of Toronto, Toronto, ON, Canada.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Binder</LastName>
<ForeName>E B</ForeName>
<Initials>EB</Initials>
<AffiliationInfo><Affiliation>Department of Translational Research in Psychiatry, Max Planck Institute of Psychiatry, Munich, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Dannlowski</LastName>
<ForeName>U</ForeName>
<Initials>U</Initials>
<AffiliationInfo><Affiliation>Department of Psychiatry, University of Münster, Münster, Germany.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Psychiatry, University of Marburg, Marburg, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Ingelman-Sundberg</LastName>
<ForeName>M</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Section of Pharmacogenetics, Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.</Affiliation>
</AffiliationInfo>
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<Language>eng</Language>
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   |texte=   Elevated CYP2C19 expression is associated with depressive symptoms and hippocampal homeostasis impairment.
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	Serveur d'exploration sur les relations entre la France et l'Australie
	Attention, ce site est en cours de développement ! Attention, site généré par des moyens informatiques à partir de corpus bruts. Les informations ne sont donc pas validées.

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Elevated CYP2C19 expression is associated with depressive symptoms and hippocampal homeostasis impairment.

Elevated CYP2C19 expression is associated with depressive symptoms and hippocampal homeostasis impairment.

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