The Brown Center for the Study of Children at Risk

The Brown Center for the Study of Children at Risk

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Conradt E.,University of Utah | Fei M.,The Brown Center for the Study of Children at Risk | LaGasse L.,The Brown Center for the Study of Children at Risk | LaGasse L.,Brown University | And 6 more authors.
Frontiers in Behavioral Neuroscience | Year: 2015

We examined whether placental DNA methylation of the glucocorticoid receptor gene, NR3C1 was associated with self-regulation and neuroendocrine responses to a social stressor in infancy. Placenta samples were obtained at birth and mothers and their infants (n = 128) participated in the still-face paradigm when infants were 5 months old. Infant self-regulation following the still-face episode was coded and pre-stress cortisol and cortisol reactivity was assessed in response to the still-face paradigm. A factor analysis of NR3C1 CpG sites revealed two factors: one for CpG sites 1-4 and the other for sites 5-13. DNA methylation of the factor comprising NR3C1 CpG sites 5-13 was related to greater cortisol reactivity and infant self-regulation, but cortisol reactivity was not associated with infant self-regulation. The results reveal that prenatal epigenetic processes may explain part of the development of infant self-regulation. © 2015 Conradt, Fei, LaGasse, Tronick, Guerin, Gorman, Marsit and Lester.


PubMed | University of Utah, The Brown Center for the Study of Children at Risk and University of Massachusetts Amherst
Type: Journal Article | Journal: Child development | Year: 2016

This study tested whether maternal responsiveness may buffer the child to the effects of maternal depressive symptoms on DNA methylation of NR3C1, 11-HSD2, and neuroendocrine functioning. DNA was derived from buccal epithelial cells and prestress cortisol was obtained from the saliva of 128 infants. Mothers with depressive symptoms who were more responsive and who engaged in more appropriate touch during face-to-face play had infants with less DNA methylation of NR3C1 and 11-HSD2 compared to mothers with depressive symptoms who were also insensitive. The combination of exposure to maternal depressive symptoms and maternal sensitivity was related to the highest prestress cortisol levels, whereas exposure to maternal depressive symptoms and maternal insensitivity was related to the lowest prestress cortisol levels.

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