The perinatal period, particularly pregnancy, is a period of high risk for the development and recurrence of depression (Howard and Khalifeh, 2020). Prior to the COVID-19 pandemic, 10–20 % of pregnant individuals reported clinically significant depressive symptoms (Van Niel and Payne, 2020), with prevalence rates increasing up to 27 % during the pandemic (Hessami et al., 2022; Shorey et al., 2021; Tomfohr-Madsen et al., 2021). Prenatal depressive symptoms are linked to a host of negative child outcomes, including a higher risk of adverse infant delivery outcomes (Dadi et al., 2020), poorer child cognitive development (Faleschini et al., 2019), and an increased risk for subsequent child and adult mental health issues (Faisal-Cury and Menezes, 2012; Van den Bergh et al., 2020). Exposure to depressive symptoms in-utero has also been associated with poorer socioemotional trajectories in childhood, including adverse temperament outcomes (Melchior et al., 2012; Rigato et al., 2022).

Infant temperament, defined as individual differences in emotional reactivity and self-regulation (Shiner et al., 2012), is a known predictor of adult personality (Rothbart et al., 2000). Temperament is relatively stable from birth (Rothbart, 1986) but developmental maturation and postpartum influences (i.e., postpartum depression) can lead to changes in the expression of child temperament dimensions (Putnam et al., 2006; Rothbart, 1989). Latent class trajectory analyses suggest that infants follow different developmental patterns of temperament, where certain trajectories (i.e., sharp increases in negative affectivity, as opposed to mild increases in negative affectivity) may carry an increased risk for later internalizing or externalizing behaviors by two years of age (Giesbrecht et al., 2022).

Negative affectivity (NA) is a key dimension of temperament that refers to the expression of negative emotion such as sadness, anger, distress to limitation, fear, and irritability (Rothbart, 1981). Children high in NA are more likely to exhibit emotional dysregulation and prolonged experiences of aversive emotional states (Phillips et al., 2002; Watson and Clark, 1984). Further, parent-reported NA is one of the earliest predictors of poor mental health in children (Kozlova et al., 2020). This is critical given that heightened internalizing and externalizing symptomatology in young children is predictive of depression in adolescence and adulthood (Loth et al., 2014; Mesman et al., 2001). Consequently, understanding risk and protective factors that predict elevated child NA is important for prevention and intervention efforts.

Higher levels of depressive symptoms during pregnancy are associated with increased NA in children from infancy through adolescence (Glynn et al., 2018; Rouse and Goodman, 2014; Takegata et al., 2021). However, the unique contributions of prenatal depression can be challenging to disentangle from postpartum depression which often follows prenatal depression (Hutchens and Kearney, 2020). This is because postpartum depressive symptoms are linked to child NA through environmental stressors such as harsh parenting (Brummelte and Galea, 2016), disrupted attachment (Hentges et al., 2021; Rollè et al., 2020), poor bonding (Beato et al., 2022), and distorted perceptions of their child's behaviour (Whiffen, 1990), all of which are associated with poor child socioemotional functioning (Berthelon et al., 2020; Newman, 2017).

There is emerging evidence that elevated prenatal depressive symptoms may exert unique effects on child outcomes, like child NA, independent of postpartum depression (Thompson et al., 2021). This has been proposed to occur through physiological mechanisms, including the activation of maternal stress response networks (e.g., dysregulation in the child's hypothalamic-pituitary-adrenal (HPA) axis functioning) (Austin et al., 2005; Davis et al., 2007; Mina and Reynolds, 2014) and suboptimal brain development (e.g., reduced cortical thickness in infants to mothers with prenatal depression) (Lebel et al., 2016). However, the unique impact of prenatal depressive symptoms on child socioemotional outcomes like NA is inconsistent, with some studies solely attributing poorer child socioemotional outcomes to prenatal depression (Davis and Sandman, 2012; Luoma et al., 2001), others solely to postpartum depression (Bekkhus et al., 2011; Van Batenburg-Eddes et al., 2013), and some studies citing both (Gjerde et al., 2017). This entanglement highlights the need to consider timing (prenatal vs postnatal) and chronicity (average vs fluctuations) as distinct dimensions of maternal risk (Caravale et al., 2017; Thompson et al., 2021). Examining patterns of within-person change in depressive symptoms across pregnancy and postpartum may provide clearer insight into how trajectories of maternal depressive symptoms may shape child NA.

These complexities may also help explain the significant variability in the strength of the observed associations between prenatal depressive symptoms and child NA, with estimates ranging from small (r = 0.17) (Spry et al., 2020) to moderate (r = 0.39) (Rouse and Goodman, 2014). In parallel, recent research has revealed several developmental trajectories of child NA with some infants showing sharp increases in NA, while others demonstrated decreases, or mild increases in NA over time (Giesbrecht et al., 2022). This heterogeneity suggests the presence of other factors that may moderate the influence of prenatal depressive symptoms, helping to explain why some children show greater risk or resilience than others. Identifying potential moderators may provide a direct target of intervention to mitigate the risk typically associated with prenatal depressive symptoms.

A potential child-related moderator of prenatal depressive symptoms and child NA is infant sleep duration. Infants spend much of their early life asleep; and longer infant sleep duration has been associated with improved physical (Pecora et al., 2022; Tham et al., 2017), cognitive (Smithson et al., 2018; Tham et al., 2017), and socioemotional developmental outcomes (Chaput et al., 2017; Pecora et al., 2022). While shorter infant sleep duration is reliably linked with higher parent reported levels of infant NA (Bouvette-Turcot et al., 2015; Morales-Munoz et al., 2020), the relationship between infant sleep and child NA is likely bidirectional, such that chronic infant sleep difficulties may also exacerbate levels of NA (Sadeh et al., 1994; Spruyt et al., 2008). For example, one study found that when infant sleep variability was high (i.e., more night-to-night changes in sleep measures within an individual), higher levels of postnatal depressive symptoms on infant NA were associated with higher levels of child NA (Parade et al., 2019). Similarly, another study found that higher levels of prenatal depressive symptoms were associated with less local brain connectivity, but only in infants with lower sleep duration (Donnici et al., 2023). Infant sleep is a modifiable factor that may explain variability in the impact of prenatal depressive symptoms on child NA, helping identify why some infants are more vulnerable than others. A deeper understanding of these relationships may guide early interventions to reduce the impact of prenatal depression on child development.