Neural Signaling of Cortisol, Childhood Emotional Abuse, and Depression-Related Memory Bias.

Neural Signaling of Cortisol, Childhood Emotional Abuse, and Depression-Related Memory Bias.
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DOI:
10.1016/j.bpsc.2017.11.005
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发表时间:
2018-03
期刊:
Biological psychiatry. Cognitive neuroscience and neuroimaging
影响因子:
--
通讯作者:
Birn RM
Birn RM
中科院分区:
其他
文献类型:
--
作者:
Abercrombie HC;Frost CP;Walsh EC;Hoks RM;Cornejo MD;Sampe MC;Gaffey AE;Plante DT;Ladd CO;Birn RM

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Cortisol has potent effects on learning and neuroplasticity, but little is known about its effects on negative memory biases in depression. Animal models show that aversive caregiving alters effects of glucocorticoids (primarily corticosterone in rodents; cortisol in primates) on learning and neuroplasticity into adulthood. We investigated whether history of childhood emotional abuse (EA) moderated effects of cortisol administration (CORT) vs. placebo on emotional memory formation in depression. Participants included 75 unmedicated women with varying levels of depression severity and/or EA history. In a double-blind crossover investigation, we used fMRI to measure effects of CORT (vs. Placebo) on neural function during emotional memory formation. CORT eliminated the well-known relation between depression severity and negative memory bias, a finding explained by EA severity. For women with history of severe EA, CORT reduced depression-related negative memory bias and normalized recall for pleasant stimuli. EA severity also moderated CORT’s effects on neural function: in women with history of severe EA, CORT increased activation in supplementary motor area (SMA) during unpleasant relative to pleasant pictures. Additionally, SMA activation predicted reduced negative bias for pictures encoded during CORT. These results suggest that increasing cortisol signaling may be neurocognitively beneficial in depressed women with history of maltreatment. The findings corroborate prior research suggesting that presence or absence of adverse caregiving is etiologically important in depression. The findings suggest potential neurocognitive mechanisms of therapeutics targeting cortisol signaling, which show promise in treating affective disorders.
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