Neurobehavioral abnormalities following prenatal psychosocial stress are differentially modulated by maternal environment

Author:

Zoubovsky Sandra P.ORCID,Williams Michael T.ORCID,Hoseus Sarah,Tumukuntala Shivani,Riesenberg Amy,Schulkin Jay,Vorhees Charles V.ORCID,Campbell Kenneth,Lim Hee-WoongORCID,Muglia Louis J.ORCID

Abstract

AbstractPrenatal stress (PS) is associated with increased vulnerability to affective disorders. Transplacental glucocorticoid passage and stress-induced maternal environment alterations are recognized as potential routes of transmission that can fundamentally alter neurodevelopment. However, molecular mechanisms underlying aberrant emotional outcomes or the individual contributions intrauterine stress versus maternal environment play in shaping these mechanisms remain unknown. Here, we report anxiogenic behaviors, anhedonia, and female hypothalamic-pituitary-adrenal axis hyperactivity as a consequence of psychosocial PS in mice. Evidence of fetal amygdala programming precedes these abnormalities. In adult offspring, we observe amygdalar transcriptional changes demonstrating sex-specific dysfunction in synaptic transmission and neurotransmitter systems. We find these abnormalities are primarily driven by in-utero stress exposure. Importantly, maternal care changes postnatally reverse anxiety-related behaviors and partially rescue gene alterations associated with neurotransmission. Our data demonstrate the influence maternal environment exerts in shaping offspring emotional development despite deleterious effects of intrauterine stress.

Funder

U.S. Department of Health & Human Services | NIH | National Institute of General Medical Sciences

Cincinnati Children’s Research Foundation

University of Cincinnati Office of Vice President for Research

Publisher

Springer Science and Business Media LLC

Subject

Biological Psychiatry,Cellular and Molecular Neuroscience,Psychiatry and Mental health

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