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Published on: June 13, 2021
Hypothalamic-pituitary-adrenal (HPA) axis function in 3-month old infants with prenatal selective serotonin reuptake
Tim F Oberlander1, Ruth Grunau, Linda Mayes
1Department of Pediatrics, UBC, Vancouver, BC, Canada V6H 3V4. toberlander@cw.bc.ca
Insights
Prenatal exposure to selective serotonin reuptake inhibitors (SSRIs) alters infant stress response and lowers evening cortisol. These effects suggest early programming of the hypothalamic-pituitary-adrenal (HPA) system, influenced by maternal mood and caregiving.
Area of Science:
- Neuroendocrinology
- Developmental Psychology
- Pharmacology
Background:
- Prenatal stress and SSRI exposure impact offspring HPA axis reactivity.
- The combined effects on infant HPA activity remain largely unknown.
Purpose of the Study:
- To investigate HPA axis basal levels and stress responsiveness in 3-month-old infants with prenatal SSRI exposure.
- To understand the influence of feeding method and maternal mood on these responses.
Main Methods:
- Compared salivary cortisol levels in infants exposed to SSRIs prenatally versus controls.
- Assessed cortisol under basal and stress-challenge conditions (habituation task).
- Controlled for feeding method and maternal mood (pre- and postnatal).
Main Results:
- Prenatal SSRI exposure was associated with lower early evening basal cortisol levels.
- Stress reactivity differences emerged when accounting for the moderating effect of feeding method.
- No association found between postnatal SSRI exposure via breast milk and cortisol levels.
Conclusions:
- Prenatal SSRI exposure alters HPA stress response patterns and basal cortisol.
- Feeding method moderates stress challenge HPA response differences.
- Findings suggest early programming of the HPA system by antenatal/postnatal factors.
Background:
Prenatal exposure to stress and selective serotonin reuptake inhibitors (SSRIs) alter hypothalamic-pituitary-adrenal (HPA) stress reactivity in offspring, however, the effects of combined exposure to HPA activity in human infants is unknown.
Objective:
To examine HPA basal levels and stress responsiveness in 3-month olds with prenatal exposure to SSRIs.
Methods:
Salivary cortisol levels in infants of SSRI treated mothers (n=31, mean exposure 230.2+/-72.2 days) were compared with non-SSRI exposed (n=45) infants in response to a challenge (infant-controlled habituation task) and under basal conditions in the late afternoon/early evening. Mode of feeding, to account for possible postnatal drug exposure via breast milk, as well as measures of pre and postnatal maternal mood, were included as covariates.
Results:
Lower post-stress cortisol levels were observed in non-SSRI exposed/non-breastfed infants compared with non-SSRI exposed infants who were breastfed at 3 months of age. Stress reactivity patterns among SSRI exposed infants did not differ with mode of feeding. The cortisol reactivity slope (CRS) was significantly lower among non-SSRI exposed non-breastfed infants compared with non-SSRI exposed breastfed infants. Early evening basal cortisol levels were lower in SSRI exposed infants than in non-SSRI exposed infants, controlling for maternal mood and mode of feeding. Postnatal SSRI exposure (infant SSRI drug levels) via breast milk was not associated with stress or basal cortisol levels. Total cortisol, reflected by the AUC measure, did not differ significantly between exposure groups.
Conclusions:
Prenatal SSRI exposure altered HPA stress response patterns and reduced early evening basal cortisol levels. Stress challenge HPA response differences only became apparent when the moderating effect of method of feeding was accounted for. These findings suggest an early "programming" effect of antenatal maternal mood, prenatal SSRI exposure and postnatal maternal care giving on the HPA system.
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