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Using a Murine Model of Psychosocial Stress in Pregnancy as a Translationally Relevant Paradigm for Psychiatric Disorders in Mothers and Infants
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Maternal prenatal cortisol programs the infant hypothalamic-pituitary-adrenal axis.
Jessica L Irwin1, Amy L Meyering2, Gage Peterson3
1Department of Psychology, University of La Verne, La Verne, CA 91750, United States; Department of Psychology, Chapman University, Orange, CA 92866, United States.
Psychoneuroendocrinology
|December 19, 2020
Summary
Maternal prenatal cortisol exposure is linked to infant stress responses. Elevated maternal cortisol during pregnancy was associated with greater infant cortisol reactivity to inoculation pain at 6 and 12 months.
Area of Science:
- Endocrinology
- Developmental Psychology
- Neuroscience
Background:
- Maternal glucocorticoids are implicated in fetal programming.
- Prenatal exposure to elevated glucocorticoids affects offspring hypothalamic-pituitary-adrenal (HPA) axis function in animal models.
- Limited human data exist on maternal cortisol during pregnancy and infant cortisol reactivity.
Purpose of the Study:
- To investigate the association between maternal prenatal cortisol trajectories and infant cortisol reactivity.
- To examine the impact of maternal stress hormones on the developing infant HPA axis.
Main Methods:
- Longitudinal study of 152 mother-infant pairs.
- Measurement of maternal cortisol levels during pregnancy.
- Assessment of infant cortisol reactivity to inoculation pain at 6 and 12 months of age.
Main Results:
- Elevated prenatal maternal cortisol was associated with increased infant cortisol response to inoculation.
- This association was observed at both 6 and 12 months postpartum.
- Findings suggest a link between maternal prenatal stress hormones and infant HPA axis programming.
Conclusions:
- Prenatal maternal cortisol exposure influences the development of the infant HPA axis.
- Maternal stress during pregnancy may have lasting effects on infant stress reactivity.
- This study provides direct human evidence for fetal programming of the HPA axis by maternal glucocorticoids.
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