Abstract
Exposure to prenatal and early-life stress results in alterations in neural connectivity and an increased risk for neuropsychiatric disorders. In particular, alterations in amygdala connectivity have emerged as a common effect across several recent studies. However, the impact of prenatal stress exposure on the functional organization of the amygdala has yet to be explored in the prematurely-born, a population at high risk for neuropsychiatric disorders.We test the hypothesis that preterm birth and prenatal exposure to maternal stress alter functional connectivity of the amygdala using two independent cohorts. The first cohort is used to establish the effects of preterm birth and consists of 12 very preterm neonates and 25 term controls, all without prenatal stress exposure. The second is analyzed to establish the effects of prenatal stress exposure and consists of 16 extremely preterm neonates with prenatal stress exposure and 10 extremely preterm neonates with no known prenatal stress exposure. Standard resting-state functional magnetic resonance imaging and seed connectivity methods are used.When compared to term controls, very preterm neonates show significantly reduced connectivity between the amygdala and the thalamus, the hypothalamus, the brainstem, and the insula (p < 0.05). Similarly, when compared to extremely preterm neonates without exposure to prenatal stress, extremely preterm neonates with exposure to prenatal stress show significantly less connectivity between the left amygdala and the thalamus, the hypothalamus, and the peristriate cortex (p < 0.05). Exploratory analysis of the combined cohorts suggests additive effects of prenatal stress on alterations in amygdala connectivity associated with preterm birth.Functional connectivity from the amygdala to other subcortical regions is decreased in preterm neonates compared to term controls. In addition, these data, for the first time, suggest that prenatal stress exposure amplifies these decreases.
Highlights
Preterm birth, birth before 37 weeks gestation, alters connectivity in the developing brain (Allievi et al, 2016; Karolis et al, 2016; Kwon et al, 2016; Smyser et al, 2016)
Preterm neonates with no prenatal stress exposure had significantly lower gestational ages and birth weights compared to the group with prenatal stress exposure (p = 0.04 and p = 0.01, respectively), but there were no significant differences in sex, race, postmenstrual age at scan and perinatal morbidities
We provide evidence that preterm birth and prenatal exposure to maternal stress alter amygdala connectivity assessed in the neonatal period
Summary
Birth before 37 weeks gestation, alters connectivity in the developing brain (Allievi et al, 2016; Karolis et al, 2016; Kwon et al, 2016; Smyser et al, 2016) While these alterations have been largely attributed to postnatal perturbations (Brummelte et al, 2012; Pineda et al, 2014; Rogers et al, 2016; Smith et al, 2011; Smyser et al, 2013), emerging data suggest that prenatal exposure to maternal stress may play a role (Bronson and Bale, 2014; Chen and Baram, 2016; Constantinof et al, 2015; Provencal and Binder, 2015). Preliminary findings in preterm neonates (Rogers et al, 2015) and young adults (Papini et al, 2014) suggest reduced amygdala connectivity to subcortical, limbic, and frontal regions Following these studies, using resting-state functional MRI (fMRI), we test the hypothesis that prenatal exposure to maternal stress reduces functional connectivity of the amygdala with these regions in preterm infants. These results suggest that reduction in amygdala connectivity associated with preterm birth is moderated by exposure to prenatal stress
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