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Early developmental emergence of human amygdala-prefrontal connectivity after maternal deprivation
Dylan G Gee1, Laurel J Gabard-Durnam, Jessica Flannery
1Departments of Psychology and Psychiatry and Biobehavioral Services, University of California, Los Angeles, CA 90095.
Insights
Early adversity, like maternal deprivation, accelerates brain development in children, leading to mature medial prefrontal cortex (mPFC) and amygdala connections. This adaptation, mediated by cortisol, may reduce anxiety despite higher overall levels.
Area of Science:
- Neuroscience
- Developmental Psychology
- Endocrinology
Background:
- Medial prefrontal cortex (mPFC) and amygdala connectivity matures from childhood to adolescence.
- Maternal deprivation in rodents accelerates this neurodevelopmental trajectory.
- Early institutionalization in humans serves as a model for early maternal deprivation.
Purpose of the Study:
- To investigate amygdala-mPFC connectivity phenotypes in previously institutionalized youths.
- To explore the role of cortisol and the hypothalamic-pituitary-adrenal axis in mediating these changes.
- To understand the adaptive significance of accelerated neurodevelopment in response to early adversity.
Main Methods:
- Functional connectivity analysis of amygdala-mPFC circuits.
- Assessment of cortisol levels and hypothalamic-pituitary-adrenal axis activity.
- Comparison of connectivity patterns between previously institutionalized children and comparison groups.
Main Results:
- Previously institutionalized children showed mature, negative amygdala-mPFC coupling, unlike comparison children's immature, positive coupling.
- This mature connectivity pattern resembled the adolescent phenotype.
- Cortisol mediated the observed connectivity, indicating stress-induced HPA axis influence.
- Negative coupling conferred some anxiety reduction, though anxiety remained elevated in the institutionalized group.
Conclusions:
- Accelerated amygdala-mPFC development is an ontogenetic adaptation to early life stress.
- Stress hormones like cortisol play a crucial role in shaping brain circuitry development.
- This neurodevelopmental adaptation may offer partial protection against anxiety in the context of early adversity.
Abstract:
Under typical conditions, medial prefrontal cortex (mPFC) connections with the amygdala are immature during childhood and become adult-like during adolescence. Rodent models show that maternal deprivation accelerates this development, prompting examination of human amygdala-mPFC phenotypes following maternal deprivation. Previously institutionalized youths, who experienced early maternal deprivation, exhibited atypical amygdala-mPFC connectivity. Specifically, unlike the immature connectivity (positive amygdala-mPFC coupling) of comparison children, children with a history of early adversity evidenced mature connectivity (negative amygdala-mPFC coupling) and thus, resembled the adolescent phenotype. This connectivity pattern was mediated by the hormone cortisol, suggesting that stress-induced modifications of the hypothalamic-pituitary-adrenal axis shape amygdala-mPFC circuitry. Despite being age-atypical, negative amygdala-mPFC coupling conferred some degree of reduced anxiety, although anxiety was still significantly higher in the previously institutionalized group. These findings suggest that accelerated amygdala-mPFC development is an ontogenetic adaptation in response to early adversity.
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