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

ABSTRACT: Prenatal 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 dysfunctio

SUBMITTER: Zoubovsky SP 

PROVIDER: S-EPMC8764031 | biostudies-literature | 2022 Jan

REPOSITORIES: biostudies-literature