Abstract

The third trimester of pregnancy represents a sensitive phase for infant brain plasticity when a series of fast-developing cellular events (synaptogenesis, neuronal migration, and myelination) regulates the development of neural circuits. Throughout this dynamic period of growth and development, the human brain is susceptible to stress. Preterm infants are born with an immature brain and are, while admitted to the neonatal intensive care unit, precociously exposed to stressful procedures. Postnatal stress may contribute to altered programming of the brain, including key systems such as the hypothalamic–pituitary–adrenal axis and the autonomic nervous system. These neurobiological systems are promising markers for the etiology of several affective and social psychopathologies. As preterm birth interferes with early development of stress-regulatory systems, early interventions might strengthen resilience factors and might help reduce the detrimental effects of chronic stress exposure. Here we will review the impact of stress following premature birth on the programming of neurobiological systems and discuss possible stress-related neural circuits and pathways involved in resilience and vulnerability. Finally, we discuss opportunities for early intervention and future studies.

Highlights

  • The third trimester of pregnancy represents a sensitive phase for infant brain plasticity, as a series of fast-developing cellular events, such as synaptogenesis, neuronal migration, and myelination regulate the development of neural circuits [1]

  • The reviewed literature suggests that stress has both proximate and long-lasting detrimental effects on brain and behavior in preterm-born individuals

  • How do postnatal stressor type, timing, and duration translate to changes in neurobiological systems and subsequent outcome across the life course? 2

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Summary

INTRODUCTION

The third trimester of pregnancy represents a sensitive phase for infant brain plasticity, as a series of fast-developing cellular events, such as synaptogenesis, neuronal migration, and myelination regulate the development of neural circuits [1]. Brummelte and colleagues could distinguish a period of increased vulnerability, namely early procedural pain [i.e., before scan 1 (median 32.1 weeks of gestation)] had a stronger association with white matter maturation compared to later stress (around term equivalent age), whereas subcortical gray matter showed sustained sensitivity toward neonatal stress [120]. These results are in line with findings from another study, where they reported that functional and structural connectivity patterns were affected following exposure to early (i.e., from birth to scan 1), but not late neonatal stress [i.e., scan 1 to scan 2 [termequivalent age]]. Similar findings were observed in preterm infants, namely preterm born infants’ degree of respiratory sinus arrhythmia (RSA) was positively associated with their social competence, whereas lower (mean) heart rate was associated with less behavioral problems and TABLE 1 | Neonatal stress and neurobiological systems

CONCLUDING REMARKS
75. Hevner
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