Monitoring the acute stress response and its aftermath using combined fMRI/endocrine measurements

Understanding the translation of subjective stressful experiences into neuroendocrine responses is still incomplete despite evidence that repeated psychosocial stress increases the risk for affective disorders. We reported that hippocampal resting connectivity predicts the HPA axis tone [1], and hippocampal/orbitofrontal deactivation seems a central signature of the initiation of the acute stress response [2]. Subjects' hippocampal response to a memory task were further predictive of their acute endocrine response [3]. Here we focus on the temporal dynamics of the stress response in 40 healthy subjects, employing a variant of the Montreal Imaging Stress Test [2] in which psychosocial stress (cognitive overload, evaluative threat) is exerted and cessated during a calculation task in a controlled way. We hypothesize that individuals not only differ in the intensity of their limbic response but also in their time needed to 'shut down' this pattern after the peracute phase. This could explain variance of the acute cortisol response and their HPA axis tone. We extend previous approaches [2,3] by functional connectivity analysis including critical limbic/hypothalamic connections. The interrelation with hippocampal responses during memory tasks will be studied by employing an encoding/recognition task with and without interference by the stress paradigm. [1] Kiem et al. PNEC 2013 [2] Pruessner et al. Biol Psychiatry 2008;63:234 – 40 [3] Khalili-Mahani et al. Hippocampus 2010;20:323 – 34