Early developmental emergence of human amygdala–prefrontal connectivity after maternal deprivation

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...

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Published in:	Proceedings of the National Academy of Sciences - PNAS 2013-09, Vol.110 (39), p.15638-15643
Main Authors:	Gee, Dylan G., Gabard-Durnam, Laurel J., Flannery, Jessica, Goff, Bonnie, Humphreys, Kathryn L., Telzer, Eva H., Hare, Todd A., Bookheimer, Susan Y., Tottenham, Nim
Format:	Article
Language:	eng
Subjects:	Adolescent Adolescents Aging Amygdala Amygdala - growth & development Amygdala - physiopathology Anatomical correlates of behavior Animal behavior Anxiety, Separation - physiopathology Behavioral neuroscience Behavioral psychophysiology Biological and medical sciences Brain Child Child development Child, Preschool Connectivity Developmental biology Developmental psychology Fear Fundamental and applied biological sciences. Psychology Genotype & phenotype Humans Hydrocortisone - metabolism Institutionalization Magnetic Resonance Imaging Maternal Deprivation Nerve Net - growth & development Nerve Net - physiopathology Phenotype Phenotypes Prefrontal Cortex - growth & development Prefrontal Cortex - physiopathology Psychological stress Psychology. Psychoanalysis. Psychiatry Psychology. Psychophysiology Reactivity Separation anxiety Social Sciences
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Summary:	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.
ISSN:	0027-8424 1091-6490