Social evaluative threat (SET) is a potent stressor in humans linked to autonomic and endocrine responses, and multiple health problems. Neuroimaging has recently begun to elucidate the brain correlates of SET, but as yet little is known about the mediating cortical-brainstem pathways in humans. This paper replicates and extends findings in a companion paper (Wager et al., submitted) using an independent cohort of participants and different image acquisition parameters. Here, we focused specifically on relationships between the medial prefrontal cortex (MPFC), midbrain periaqueductal gray (PAG), and heart rate (HR). We applied multi-level path analysis to localize brain mediators of SET effects on HR and self-reported anxiety. HR responses were mediated by opposing signals in two distinct sub-regions of the MPFC—increases in rostral dorsal anterior cingulate cortex (rdACC) and deactivation in ventromedial prefrontal cortex (vmPFC). In addition, HR responses were mediated by PAG. Additional path analyses provided support for two cortical subcortical pathways: one linking vmPFC, PAG, and HR, and another linking rdACC, thalamus, and HR. PAG responses were linked with HR changes both before and during SET, whereas cortical regions showed stronger connectivity with HR during threat. Self-reported anxiety showed a partially overlapping, but weaker, pattern of mediators, including the vmPFC, dorsomedial PFC (dmPFC), and lateral frontal cortex, as well as substantial individual differences that were largely unexplained. Taken together, these data suggest pathways for the translation of social threats into both physiological and experiential responses, and provide targets for future research on the generation and regulation of emotion.

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Research in nonhuman animals suggests that reactivation can induce a transient, unstable state in a previously consolidated memory, during which the memory can be disrupted or modified, necessitating a process of restabilization in order to persist. Such findings have sparked a wave of interest into whether this phenomenon, known as reconsolidation, occurs in humans. Translating research from animal models to human experiments and even to clinical interventions is an exciting prospect, but amid this excitement, relatively little work has critically evaluated and synthesized existing research regarding human memory reconsolidation. In this review, we formalize a framework for evaluating and designing studies aiming to demonstrate human memory reconsolidation. We use this framework to shed light on reconsolidation-based research in human procedural memory, aversive and appetitive memory, and declarative memory, covering a diverse selection of the most prominent examples of this research, including studies of memory updating, retrieval-extinction procedures, and pharmacological interventions such as propranolol. Across different types of memory and procedure, there is a wealth of observations consistent with reconsolidation. Moreover, some experimental findings are already being translated into clinically relevant interventions. However, there are a number of inconsistent findings, and the presence of alternative explanations means that we cannot conclusively infer the presence of reconsolidation at the neurobiological level from current evidence. Reconsolidation remains a viable but hotly contested explanation for some observed changes in memory expression in both humans and animals. Developing effective and efficient new reconsolidation-based treatments can be a goal that unites researchers and guides future experiments. (PsycINFO Database Record

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Real-life shooting decisions typically occur under acute threat and require fast switching between vigilant situational assessment and immediate fight-or-flight actions. Recent studies suggested that freezing facilitates action preparation and decision-making but the neurocognitive mechanisms remain unclear. We applied functional magnetic resonance imaging, posturographic and autonomic measurements while participants performed a shooting task under threat of shock. Two independent studies, in unselected civilians (N = 22) and police recruits (N = 54), revealed that preparation for shooting decisions under threat is associated with postural freezing, bradycardia, midbrain activity (including the periaqueductal gray-PAG) and PAG-amygdala connectivity. Crucially, stronger activity in the midbrain/PAG during this preparatory stage of freezing predicted faster subsequent accurate shooting. Finally, the switch from preparation to active shooting was associated with tachycardia, perigenual anterior cingulate cortex (pgACC) activity and pgACC-amygdala connectivity. These findings suggest that threat-anticipatory midbrain activity centred around the PAG supports decision-making by facilitating action preparation and highlight the role of the pgACC when switching from preparation to action. These results translate animal models of the neural switch from freeze-to-action. In addition, they reveal a core neural circuit for shooting performance under threat and provide empirical evidence for the role of defensive reactions such as freezing in subsequent action decision-making.

Response inhibition is a hallmark of executive control and crucial to support flexible behavior in a constantly changing environment. Recently, it has been shown that response inhibition is influenced by the presentation of emotional stimuli (Verbruggen and De Houwer, 2007). Healthy individuals typically differ in the degree to which they are able to regulate their emotional state, but it remains unknown whether individual differences in emotion regulation (ER) may alter the interplay between emotion and response inhibition. Here we address this issue by testing healthy volunteers who were equally divided in groups with high and low heart rate variability (HRV) during rest, a physiological measure that serves as proxy of ER. Both groups performed an emotional stop-signal task, in which negative high arousing pictures served as negative emotional stimuli and neutral low arousing pictures served as neutral non-emotional stimuli. We found that individuals with high HRV activated and inhibited their responses faster compared to individuals with low HRV, but only in the presence of negative stimuli. No group differences emerged for the neutral stimuli. Thus, individuals with low HRV are more susceptible to the adverse effects of negative emotion on response initiation and inhibition. The present research corroborates the idea that the presentation of emotional stimuli may interfere with inhibition and it also adds to previous research by demonstrating that the aforementioned relationship varies for individuals differing in HRV. We suggest that focusing on individual differences in HRV and its associative ER may shed more light on the dynamic interplay between emotion and cognition.

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Our results suggest a protective role for the ability to integrate memories in their original visual learning context against the development of PTSD symptoms.