Social scaffolding of human amygdala-mPFCcircuit development

Abstract

Strong evidence indicates that reciprocal connections between the amygdala and medial prefrontal cortex (mPFC) support fundamental aspects of emotional behavior in adulthood. However, this circuitry is slow to develop in humans, exhibiting immaturity in childhood. The argument is made that the development of this circuitry in humans is intimately associated with caregiving, such that parental availability during childhood provides important and enduring scaffolding of neuroaffective processes that ultimately form of the nature of the adult phenotype.

Neurobiology of infant attachment: attachment despite adversity and parental programming of emotionality

“…Finally, a common theme in recent literature is emerging in which it is proposed that caregiver adversity promotes accelerated infant development via premature closure of sensitive periods [13,33]. While this may be true in some instances, we argue that this conceptualization is too simplistic and has the potential to dissuade researchers from exploring alternative hypotheses, thus limiting our understanding of neurobiological pathways to pathology.…”

“…Recent research in humans suggests that the quality of parental care is critical to infant emotional development, due in part to their pronounced ability to regulate infant behavior and physiology [13,14]. For example, parental presence regulates stress hormones [15,16] and brain activity in children [17,18], but not adolescents [18,19].…”

Neuroanatomical Substrates of Rodent Social Behavior: The Medial Prefrontal Cortex and Its Projection Patterns

“…The identified brain regions largely belong to the limbic system and form a complex network of diverse neural circuits related to emotional responses, appetite, sexual behavior, addiction and motivation, and social memory (Tottenham, 2015). Notably, the mPFC has emerged as a crucial neural substrate of social cognition and behaviors in humans (Dolan, 2002; Wise, 2008; Krueger et al, 2009; Grossmann, 2013; Bicks et al, 2015).…”

Maternal buffering beyond glucocorticoids: impact of early life stress on corticolimbic circuits that control infant responses to novelty

“…odor in rat dams) to regulate this aspect of infant brain function follows a specific developmental course, with decreased maternal effectiveness to reduce/buffer her infant's stress response coinciding with the infant's ability to independently locomote and leave the nest. Primate species also show maternal buffering of stress responses in infants and juveniles, which are thought to involve modulation of developing self-regulatory systems, including amygdala-prefrontal circuits (Gee et al, 2014; Gunnar et al, 2015; Gunnar and Sullivan, 2016; Sanchez et al, 2015; Tottenham 2015). The quality of maternal care can affect not only the buffering power of the mother's presence, as we have demonstrated for macaques (Sanchez et al, 2015), but can impact the way these self-regulatory systems mature, with some evidence suggesting accelerated maturation of self-regulatory processes under poor caregiving experiences, interpreted as an accelerated transition to the offspring's independent state, although also linked to enhanced emotional reactivity (Gee et al, 2013).…”