DRD2 and SLC6A3 moderate impact of maternal depressive symptoms on infant cortisol
Jaclyn A Ludmer1, Robert Levitan2, Andrea Gonzalez3
1Department of Psychology, Ryerson University, 350 Victoria Street, M5B 2K3, Toronto, Ontario, Canada.
Insights
Maternal depression impacts infant cortisol reactivity, influenced by specific genes (DRD2, SLC6A3). This interaction affects stress response flexibility, showing either diathesis-stress or differential susceptibility depending on the challenge.
Area of Science:
- Neuroscience
- Genetics
- Developmental Psychology
Background:
- Maternal depressive symptoms and infant genetics influence hypothalamic-pituitary-adrenal (HPA) axis functioning.
- Dopamine-related genes like DRD2 and SLC6A3 are implicated in infant HPA axis regulation.
Purpose of the Study:
- Investigate the interactive effects of maternal depressive symptoms and infant DRD2/SLC6A3 genotypes on infant cortisol reactivity.
- Determine if this interaction reflects diathesis-stress or differential susceptibility models.
- Examine the influence of this interaction on cortisol response flexibility across different challenges.
Main Methods:
- Community sample of 314 mother-infant dyads.
- Salivary cortisol measured at baseline, +20, and +40 min during toy frustration and maternal separation challenges.
- Maternal depressive symptoms assessed using Beck Depression Inventory-II.
- Infant buccal cells genotyped for DRD2 and SLC6A3.
Main Results:
- DRD2 and SLC6A3 genotypes moderated the relationship between maternal depressive symptoms and infant cortisol reactivity.
- Interaction followed a diathesis-stress pattern during toy frustration and differential susceptibility during maternal separation.
- Maternal depressive symptoms predicted reduced cortisol flexibility in infants with specific DRD2 (A1 allele) and SLC6A3 (10/10) genotypes.
Conclusions:
- Maternal depressive symptomatology is associated with infant cortisol reactivity and its flexibility.
- The impact of maternal depression on infant HPA axis functioning is gene-dependent.
- Findings highlight the interplay between maternal mental health, infant genetics, and early life stress response.
Abstract:
Both maternal depressive symptoms and infants' dopamine-related genetic characteristics have been linked to infants' hypothalamic-pituitary-adrenal (HPA) functioning. This study investigated the interactive influence of maternal depressive symptoms and infant DRD2 and SLC6A3 genotypes on infant cortisol reactivity; whether this interaction reflects diathesis-stress or differential susceptibility; and whether this interaction influences the flexibility of the infant cortisol response across challenges known to exert differential effects on infant cortisol reactivity. A community sample of 314 mother-infant dyads participated in toy frustration (age 16 months) and maternal separation (age 17 months) challenges, and salivary cortisol was collected at baseline, +20, and +40min. Maternal depressive symptoms were assessed with the Beck Depression Inventory-II at infant age 16 months. Infant buccal cells were collected at both time points for genotyping. DRD2 and SLC6A3 genotypes moderated the relation between maternal depressive symptomatology and infant cortisol reactivity in a diathesis-stress manner in the context of toy frustration, and in a differential susceptibility manner in the context of maternal separation. Higher levels of maternal depressive symptoms predicted reduced cortisol flexibility across challenges for infants with at least one A1 allele of DRD2 and infants with the 10/10 genotype of SLC6A3. Results suggest that maternal depressive symptomatology is related to infants' cortisol reactivity and to the flexibility of that reactivity across psychosocial challenges, but this relation is dependent on the infant's genetic characteristics.
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