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. 2016 Nov 1;6(11):e935. doi: 10.1038/tp.2016.146

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Copyright © 2016 The Author(s)

This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

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Path analysis suggests that increased inverse amygdala–prefrontal functional connectivity is a potential mechanism by which maternal distress during pregnancy enhances fetal heart rate reactivity. In the first linear regression of this path analysis, we found that maternal depressive symptoms (as measured by the Center for Epidemiological Studies Depression scale (CES-D)) was a significant predictor of connectivity between the left amygdala and the left dorsal prefrontal cortex (Amygdala–PFC, path a, beta=−0.486, P=0.009). In the second linear regression model, we found that while controlling for CES-D, Amygdala–PFC connectivity was a significant predictor of fetal heart rate reactivity (FHR reactivity, path b, beta=−0.615, P=0.020). Bias-corrected bootstrapping confirmed the significance of the indirect effect of CES-D on FHR reactivity (path c', coefficient=0.299; P=0.007).