Acute stress is associated with a sensitized amygdala. Corticosteroids, released in response to stress, are suggested to restore homeostasis by normalizing/desensitizing brain processing in the aftermath of stress. Here, we investigated the effects of corticosteroids on amygdala processing using functional magnetic resonance imaging. Since corticosteroids exert rapid nongenomic and slow genomic effects, we administered hydrocortisone either 75 min (rapid effects) or 285 min (slow effects) before scanning in a randomized, double-blind, placebo-controlled design. Seventy-two healthy males were scanned while viewing faces morphing from a neutral facial expression into fearful or happy expressions. Imaging results revealed that hydrocortisone desensitizes amygdala responsivity rapidly, while it selectively normalizes responses to negative stimuli slowly. Psychophysiological interaction analyses suggested that this slow normalization is related to an altered coupling of the amygdala with the medial prefrontal cortex. These results reveal a temporarily fine-tuned mechanism that is critical for avoiding amygdala overshoot during stress and enabling adequate recovery thereafter.
"Firstly, the CAR may exert a slow effect on brain functional connectivity. Although a number of studies have revealed that stress and stress hormone have an acute effect on brain function and functional connectivity (Wang et al., 2005; Pruessner et al., 2008; Wager et al., 2009; Qin et al., 2009; Hermans et al., 2011; Ossewaarde et al., 2011; Veer et al., 2011), previous studies have also demonstrated that corticosteroids enhance PFC function (Henckens et al., 2011) and increase the coupling between the amygdala and the mPFC (Henckens et al., 2010) by slow, genomic changes that manifest themselves several hours after exogenous administration . These pharmacological studies, however, are not an exact copy of naturally occurring circumstances. "
"Cortisol's effects on the human brain's threat systems have however only been studied using passive threat paradigms wherein no active escape was possible [Henckens et al., 2010; Merz et al., 2010]. The question therefore arises whether cortisol can exert dissociating effects on the brain's threat systems depending on active (escape) and passive (fear) threat conditions. "
"However, the posterior hippocampus is also strongly connected to the anterior hippocampus, which is tightly linked to the amygdala [Fanselow and Dong, 2010]. These regions are all important targets of CORT, and although we did not find effects on these regions [in contrast to others, e.g., Henckens et al., 2010], we cannot exclude that CORT acted on the posterior hippocampus via these regions. Irrespective of drug condition, we did not find effects of the cry stimuli in the amygdala, which agrees with our findings using this crying paradigm in nonparental young women [Bos et al., 2010] and another finding with nonparental males [Seifritz et al., 2003]. "
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