Our research is concentrated in the following five domains:

1. Reallocation of neural resources during acute stress: One key assumption in our work is that acute stress prompts a strategic alteration in the way our brain functions. When faced with imminent threat, organisms mount a concerted response to restore homeostasis that involves central release of neurotransmitters and peripheral stress hormones. These act as neuromodulators to alter cellular properties of large-scale neuronal populations and thus exert widespread yet regionally specific effects in the brain. We have demonstrated such regionally specific effects in the amygdala, the hippocampus, the dorsolateral prefrontal cortex, and the reward system. Furthermore, we make use of recent developments in functional neuroimaging that allow for identification and quantification of connectivity among large-scale networks. Such methods have revealed a finite set of distributed networks that can be identified based on both consistent activation in model-based studies and coherent signal fluctuations in the resting brain. This set includes networks that have been associated with executive control and vigilance or salience processing. We investigate how acute stress alters the balance between such large-scale networks and what mechanisms underlie this network reorganization.

Key Publications:

  • Young, C.B., Raz, G., Everaerd,D., Beckmann, C.F., Tendolkar, I., Hendler, T., Fernández, G., & Hermans, E.J. (2017). Dynamic shifts in large-scale brain network balance as a function of arousal. Journal of Neuroscience, 37(2), 281-290.
  • Hermans, E. J., Henckens, M. J. A. G., Joëls, M., & Fernández, G. (2014). Dynamic adaptation of large-scale brain networks in response to acute stressors. Trends in Neurosciences, 37(6), 304–314.
  • Hermans, E.J., van Marle, H.J.F., Ossewaarde, L., Henckens, M.J.A.G., Qin, S., van Kesteren, M.T.R., Schoots, V.C., Cousijn, H., Rijpkema, M., Oostenveld, R., and Fernández, G. (2011). Stress-related noradrenergic activity prompts large-scale neural network reconfiguration. Science 334, 1151-1153.
  • Ossewaarde, L., Qin, S., van Marle, H.J.F., van Wingen, G.A., Fernández, G., and Hermans, E.J. (2011). Stress-induced reduction in reward-related prefrontal cortex function. NeuroImage, 55, 345-352.

2. Time dependency of effects of stress on cognition: Effects of stress on cognition are mediated by stress-sensitive neurotransmitters and hormones, such as catecholamines and corticosteroids, which act in specific temporal domains. An important question is therefore whether the actions of stress-sensitive neuromodulatory systems within these different temporal domains are also functionally different. In a series of studies, we and our colleagues have shown that the slower actions of corticosteroids often oppose the arousing and anxiogenic actions of rapid catecholaminergic activation. This work has contributed to the now widely held view that an important function of corticosteroid release is to normalize brain activity in the aftermath of stressful experiences.

Key publications:

  • Hermans, E. J., Henckens, M. J. A. G., Joëls, M., & Fernandez, G. (2016). Time-dependent shifts in neural systems supporting decision-making under stress. In J.-C. Dreher & L. Tremblay (Eds.), Decision Neuroscience: Handbook of Reward and Decision Making (2nd edition). Elsevier.
  • Hermans, E. J., Henckens, M. J. A. G., Joëls, M., & Fernández, G. (2014). Dynamic adaptation of large-scale brain networks in response to acute stressors. Trends in Neurosciences, 37(6), 304–314.
  • Henckens, M.J.A.G., Pu, Z., Hermans, E.J., van Wingen, G.A., Joëls, M., and Fernández, G. (2012). Dynamically changing effects of corticosteroids on human hippocampal and prefrontal processing. Human Brain Mapping 33(12), 2885-97.
  • Putman, P., Hermans, E.J., Koppeschaar, H., van Schijndel, A., and van Honk, J. (2007). A single administration of cortisol acutely reduces preconscious attention for fear in anxious young men. Psychoneuroendocrinology 32, 793-802.

3. Neuroendocrine regulation of memory formation: Stressful, aversive events are extremely well remembered. Such a declarative memory enhancement is evidently beneficial for survival, but the same mechanism may become maladaptive and culminate in mental diseases such as posttraumatic stress disorder (PTSD). Stress hormones are known to enhance postlearning consolidation of aversive memories but are also thought to have immediate effects on attentional, sensory, and mnemonic processes during memory encoding. Despite their significance for our understanding of the etiology of stress-related mental disorders, effects of acute stress at memory formation, and their brain correlates at the system scale, remain poorly understood. In a series of functional neuroimaging studies, we have investigated the neural correlates of memory formation following controlled experimental induction of acute stress. This work has revealed how amygdala and hippocampal function is altered during acute stress, and provides insight into the important question how memories for stressful events are qualitatively different.

Key publications:

  • de Voogd, L. D., Fernández, G., & Hermans, E. J. (2016). Disentangling the roles of arousal and amygdala activation in emotional declarative memory. Social Cognitive and Affective Neuroscience, 11(9), 1471-1480.
  • Roozendaal, B., & Hermans, E. J. (2016). Adrenal Stress Hormone Effects on Memory. In Hormones, Brain and Behavior (3rd edition). Elsevier.
  • Qin, S., Hermans, E.J., van Marle, H.J.F., and Fernández, G. (2012). Understanding low reliability of memories for neutral information encoded under stress: Alterations in memory-related activation in the hippocampus and midbrain. Journal of Neuroscience 32, 4032-4041.
  • Henckens, M.J.A.G., Hermans, E.J., Pu, Z., Joëls, M., and Fernández, G. (2009). Stressed Memories: How Acute Stress Affects Memory Formation in Humans. Journal of Neuroscience 29, 10111-10119.

4. Neural interactions underlying memory consolidation: Ongoing fluctuations within large-scale networks have been shown to persist in “offline” periods following activity. These findings imply that stress-sensitive pathways may similarly “reverberate” after a stressful event. We indeed found prolonged activation following acute stress within the “salience processing” network. Such persistent fluctuations are of particular interest in the context of memory consolidation. It is increasingly acknowledged that after initial formation, memories undergo various stages of consolidation that transform memories into neocortical representations. Such offline processes occurring over the course of consolidation have remained elusive until electrophysiological research in rodents demonstrated that task-related neuronal spiking patterns are spontaneously “replayed” during post-learning periods, and that hippocampal theta oscillations may drive binding, reactivation, and strengthening of connections between distributed neocortical representations. We have developed new methods to track spontaneous reactivations of memory representations in humans. This work has demonstrated the importance of such processes for long-term memory formation and has thereby opened new avenues for targeted interventions.

Key publications:

  • Hermans, E. J., Kanen, J. W., Tambini, A., Fernández, G., Davachi, L., & Phelps, E. A. (in press). Persistence of Amygdala-Hippocampal Connectivity and Multi-Voxel Correlation Structures During Awake Rest After Fear Learning Predicts Long-Term Expression of Fear. Cerebral Cortex.
  • de Voogd, L.D., Klumpers, F., Fernández, G., & Hermans, E.J. (2017). Intrinsic functional connectivity between amygdala and hippocampus during rest predicts enhanced memory under stress. Psychoneuroendocrinology, 75, 192-202.
  • de Voogd, L. D., Fernández, G., & Hermans, E. J. (2016). Awake reactivation of emotional memory traces through hippocampal-neocortical interactions. NeuroImage, 134, 563–572.
  • van Kesteren, M.T.R., Fernández, G., Norris, D.G., and Hermans, E.J. (2010). Persistent schema-dependent hippocampal-neocortical connectivity during memory encoding and post-encoding rest in humans. Proceedings of the National Academy of Sciences U.S.A. 107, 7550-7555.

5. Gonadal hormone action on affective circuits: Gonadal steroid hormones such as testosterone, estradiol, and progesterone, play an important role in the regulation of affective states. For instance, mood disorders are more common among women and symptoms appear to intensify in periods of hormonal instability such as the premenstrual phase. Such effects are thought to be caused by fluctuations in estradiol and progesterone levels that interact with stress-sensitive hormones and neuromodulators. Testosterone, on the other hand, appears to mainly affect motivational systems. Higher testosterone is associated with enhanced reward sensitivity, social dominance, and proneness to aggression. Such effects are often difficult to observe directly in behavior: an increased tendency to respond aggressively, for instance, may be overridden by prefrontal cortex-dependent control mechanisms. For this reason, we use functional neuroimaging to more directly investigate effects of these gonadal hormones on the neural circuitry underlying affect and affective regulation. This work has provided new insights into how testosterone and progesterone regulate affective circuits in humans.

Key publications:

  • Ossewaarde, L., van Wingen, G.A., Kooijman, S.C., Bäckström, T., Fernández, G, and Hermans, E.J. (2011). Changes in functioning of mesolimbic incentive processing circuits during the premenstrual phase. Social, Cognitive, and Affective Neuroscience 6, 612-620.
  • Hermans, E.J., Bos, P.A., Ossewaarde, L., Ramsey, N.F., Fernández, G, and Van Honk, J. (2010). Effects of exogenous testosterone on the ventral striatal BOLD response during reward anticipation in healthy women. NeuroImage 52, 277-283.
  • Hermans, E.J., Ramsey, N.F., and van Honk, J. (2008). Exogenous testosterone enhances responsiveness to social threat in the neural circuitry of social aggression in humans. Biological Psychiatry 63, 263-270
  • Hermans, E.J., Putman, P., Baas, J.M., Koppeschaar, H.P., and van Honk, J. (2006). A single administration of testosterone reduces fear-potentiated startle in humans. Biological Psychiatry 59, 872-874.


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