Maternal Cortisol Concentrations During Pregnancy and Sex-Specific Associations With Neonatal Amygdala Connectivity and Emerging Internalizing Behaviors.


Journal

Biological psychiatry
ISSN: 1873-2402
Titre abrégé: Biol Psychiatry
Pays: United States
ID NLM: 0213264

Informations de publication

Date de publication:
15 01 2019
Historique:
received: 01 03 2018
revised: 06 06 2018
accepted: 22 06 2018
pubmed: 21 8 2018
medline: 14 1 2020
entrez: 21 8 2018
Statut: ppublish

Résumé

Maternal cortisol during pregnancy has the potential to influence rapidly developing fetal brain systems that are commonly altered in neurodevelopmental and psychiatric disorders. Research examining maternal cortisol concentrations across pregnancy and offspring neurodevelopment proximal to birth is needed to advance understanding in this area and lead to insight into the etiology of these disorders. Participants were 70 adult women recruited during early pregnancy and their infants born after 34 weeks gestation. Maternal cortisol concentrations were assessed serially over 4 days in early, mid, and late gestation. Resting state functional connectivity magnetic resonance imaging of the neonatal amygdala was examined. Mothers reported on children's internalizing behavior problems at 24 months of age. Maternal cortisol concentrations during pregnancy were significantly associated with neonatal amygdala connectivity in a sex-specific manner. Elevated maternal cortisol was associated with stronger amygdala connectivity to brain regions involved in sensory processing and integration, as well as the default mode network in girls, and with weaker connectivity to these brain regions in boys. Elevated maternal cortisol was associated with higher internalizing symptoms in girls only, and this association was mediated by stronger neonatal amygdala connectivity. Normative variation in maternal cortisol during pregnancy is associated with the coordinated functioning of the amygdala soon after birth in a sex-specific manner. The identified pathway from maternal cortisol to higher internalizing symptoms in girls via alterations in neonatal amygdala connectivity may be relevant for the etiology of sex differences in internalizing psychiatric disorders, which are more prevalent in women.

Sections du résumé

BACKGROUND
Maternal cortisol during pregnancy has the potential to influence rapidly developing fetal brain systems that are commonly altered in neurodevelopmental and psychiatric disorders. Research examining maternal cortisol concentrations across pregnancy and offspring neurodevelopment proximal to birth is needed to advance understanding in this area and lead to insight into the etiology of these disorders.
METHODS
Participants were 70 adult women recruited during early pregnancy and their infants born after 34 weeks gestation. Maternal cortisol concentrations were assessed serially over 4 days in early, mid, and late gestation. Resting state functional connectivity magnetic resonance imaging of the neonatal amygdala was examined. Mothers reported on children's internalizing behavior problems at 24 months of age.
RESULTS
Maternal cortisol concentrations during pregnancy were significantly associated with neonatal amygdala connectivity in a sex-specific manner. Elevated maternal cortisol was associated with stronger amygdala connectivity to brain regions involved in sensory processing and integration, as well as the default mode network in girls, and with weaker connectivity to these brain regions in boys. Elevated maternal cortisol was associated with higher internalizing symptoms in girls only, and this association was mediated by stronger neonatal amygdala connectivity.
CONCLUSIONS
Normative variation in maternal cortisol during pregnancy is associated with the coordinated functioning of the amygdala soon after birth in a sex-specific manner. The identified pathway from maternal cortisol to higher internalizing symptoms in girls via alterations in neonatal amygdala connectivity may be relevant for the etiology of sex differences in internalizing psychiatric disorders, which are more prevalent in women.

Identifiants

pubmed: 30122286
pii: S0006-3223(18)31665-2
doi: 10.1016/j.biopsych.2018.06.023
pmc: PMC6632079
mid: NIHMS1033768
pii:
doi:

Substances chimiques

Hydrocortisone WI4X0X7BPJ

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

172-181

Subventions

Organisme : NIMH NIH HHS
ID : R01 MH096773
Pays : United States
Organisme : NIMH NIH HHS
ID : R01 MH091351
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1 TR001414
Pays : United States
Organisme : NIMH NIH HHS
ID : R00 MH091238
Pays : United States
Organisme : NICHD NIH HHS
ID : R01 HD060628
Pays : United States
Organisme : NIMH NIH HHS
ID : K99 MH111805
Pays : United States

Informations de copyright

Copyright © 2018. Published by Elsevier Inc.

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Auteurs

Alice M Graham (AM)

Department of Behavioral Neuroscience, Oregon Health & Science University, Portland, Oregon.

Jerod M Rasmussen (JM)

Development, Health and Disease Research Program, University of California, Irvine, Irvine, California.

Sonja Entringer (S)

Development, Health and Disease Research Program, University of California, Irvine, Irvine, California; Charité Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Institute of Medical Psychology, Berlin, Germany.

Elizabeth Ben Ward (E)

Department of Computer Science, University of California, Irvine, Irvine, California.

Marc D Rudolph (MD)

Department of Psychology and Neuroscience, University of North Carolina, Chapel Hill, North Carolina.

John H Gilmore (JH)

Department of Psychiatry, University of North Carolina, Chapel Hill, North Carolina.

Martin Styner (M)

Department of Psychiatry, University of North Carolina, Chapel Hill, North Carolina.

Pathik D Wadhwa (PD)

Development, Health and Disease Research Program, University of California, Irvine, Irvine, California. Electronic address: pwadhwa@uci.edu.

Damien A Fair (DA)

Department of Behavioral Neuroscience, Oregon Health & Science University, Portland, Oregon; Advanced Imaging Research Center, Oregon Health & Science University, Portland, Oregon.

Claudia Buss (C)

Development, Health and Disease Research Program, University of California, Irvine, Irvine, California; Charité Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Institute of Medical Psychology, Berlin, Germany.

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