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Risk for developing internalizing problems in early childhood is 1.5 to 2 times greater for children of mothers who experienced prenatal anxiety and depression (Madigan et al., 2018), suggesting an intergenerational transmission of affective risk. One endophenotype of internalizing risk is the error-related negativity (ERN), an event-related potential, thought to index self-monitoring (Falkenstein et al., 2000; Moser, 2017; Olvet & Hajcak, 2008), visible 0-100 ms following an incorrect behavioral response (Falkenstein et al., 1991). An enhanced ERN is linked to more anxious and depressive symptoms (e.g., Vaidyanathan et al., 2011; Holmes & Pizzagalli, 2010) and anxiety problems in offspring (Meyer et al., 2015; Suor et al., 2022) demonstrating its utility as a transdiagnostic neural marker. However, ERN during pregnancy remains uninvestigated, leaving a critical gap in our understanding of whether prenatal ERN may mark the conference of affective risk on developing offspring. In the current study, we tested whether augmented maternal ERN, in the presence of maternal depressive symptoms, indeed predicted infant risk for internalizing problems in the form of heightened negative emotion (Gartstein et al., 2012).
Ninety-three expectant mothers (N = 93) visited the laboratory during the second (M = 21.15 weeks; SD = 3.79) and third (M = 35.92 weeks; SD = 1.47) trimesters of pregnancy and at infant age 4 months (M = 4.27, SD = 0.62). EEG was recorded as mothers completed a computerized Go/No-Go task during their second trimester visit. In the third trimester, mothers reported symptoms of depression (Edinburgh Postnatal Depression Scale; Cox et al., 1987). At infant age 4 months, infants’ negative emotion (sadness, fear) was coded during a fear-eliciting paradigm (Goldsmith & Rothbart, 1999).
We tested whether second trimester ERN predicted infant sadness and fear. Further, we tested whether third trimester depressive symptoms (controlling for anxiety) moderated the association between second trimester ERN and infant outcomes. There was no main effect of ERN on infant sadness (beta = -0.02, SE(beta) = 0.06, p > .05) or fear (beta = 0.00, SE(beta) = 0.07, p > .05). Greater depressive symptoms predicted more infant sadness (beta = 0.20, SE(beta) = 0.07, p < .01) but not fear (beta = 0.03, SE(beta) = 0.07, p > .05). Most importantly, there was a significant interaction between second trimester ERN and third trimester depressive symptoms predicting infant sadness (beta = 0.04, SE(beta) = 0.15, p < .05). At low levels of prenatal depression, a larger maternal ERN predicted less infant sadness (beta = 0.34, SE(beta) = 0.14, p < 0.05). However, at high levels of prenatal depression, a larger maternal ERN predicted more infant sadness (beta = -0.37, SE(beta) = 0.16, p < 0.05). These results suggest that a larger ERN during pregnancy is associated with subsequent infant internalizing risk only when mothers also experience high levels of prenatal depressive symptoms.