Neurosci Biobehav Rev. 2024 Jun 3:105746. doi: 10.1016/j.neubiorev.2024.105746. Online ahead of print.
ABSTRACT
Early life stress has been associated with elevated risk for later psychopathology. One mechanism that may contribute to such long-term risk is alterations in amygdala development, a brain region critical to stress responsivity. Yet effects of stress on the amygdala during human infancy, a period of particularly rapid brain development, remain largely unstudied. In order to model how early stressors may affect infant amygdala development, several discrepancies across the existing literatures on early life stress among rodents and early threat versus deprivation among older human children and adults need to be reconciled. We briefly review the key findings of each of these literatures. We then consider them in light of emerging findings from studies of human infants regarding relations among maternal caregiving, infant cortisol response, and infant amygdala volume. Finally, we advance a developmental salience model of how early threat may impact the rapidly developing infant brain, a model with the potential to integrate across these divergent literatures. Future work to assess the value of this model is also proposed.
PMID:38838878 | DOI:10.1016/j.neubiorev.2024.105746
