[Raw MRI data, not defaced] Post-retrieval stress impairs subsequent memory depending on hippocampal memory trace reinstatement during reactivation

Raw dicom files as well as native space structral and functional MRI images. Data was not defaced or normalized and to protect the privacy of our participants we will hand out this data only on request

Post-retrieval stress impairs subsequent memory depending on hippocampal memory trace reinstatement during reactivation

Stress after retrieval can impair future remembering. These memory impairments may be attributed to a weakening of the original memory during reactivation-dependent reconsolidation or to the creation of competitive memory traces that can interfere with future retrieval. Although reconsolidation and interference theories predict forgetting, the neural mechanisms underlying potentially disruptive effects of post-retrieval stress on future remembering are completely unknown. Here, we used a three-day paradigm in which participants underwent functional MRI scanning during initial encoding of word-picture pairs (Day1), partial reactivation of these pairs shortly before a stress or control manipulation (Day 2), and a final cued-recall test (Day 3). Our results show that post-reactivation stress impairs subsequent memory depending on the strength of neural reinstatement of the memory trace during reactivation, as reflected in category-level reinstatement in ventrotemporal cortex (VTC), trial-wise hippocampal encoding-retrieval similarity and the connectivity of the hippocampus with the posterior cingulate cortex (PCC). Moreover, comparison of Day1 to Day3 memory representations in the PCC revealed that successful Day 3 recall was linked to Day1-Day3 pattern dissimilarity in controls, suggesting the use of a different trace, whereas stressed participants relied on the original memory representation. These neural representation changes were again dependent on VTC reinstatement during reactivation. Together, our findings suggest that the impairing effects of post-retrieval stress on future memory relate to the strength of reactivation of the original memory trace, driven by the hippocampus and its crosstalk with neocortical representation areas, revealing disruptive effects on the formation of multiple memory traces

Post-retrieval stress impairs subsequent memory depending on hippocampal memory trace reinstatement during reactivation

Stress after retrieval can impair future remembering. These memory impairments may be attributed to a weakening of the original memory during reactivation-dependent reconsolidation or to the creation of competitive memory traces that can interfere with future retrieval. Although reconsolidation and interference theories predict forgetting, the neural mechanisms underlying potentially disruptive effects of post-retrieval stress on future remembering are completely unknown. Here, we used a three-day paradigm in which participants underwent functional MRI scanning during initial encoding of word-picture pairs (Day1), partial reactivation of these pairs shortly before a stress or control manipulation (Day 2), and a final cued-recall test (Day 3). Our results show that post-reactivation stress impairs subsequent memory depending on the strength of neural reinstatement of the memory trace during reactivation, as reflected in category-level reinstatement in ventrotemporal cortex (VTC), trial-wise hippocampal encoding-retrieval similarity and the connectivity of the hippocampus with the posterior cingulate cortex (PCC). Moreover, comparison of Day1 to Day3 memory representations in the PCC revealed that successful Day 3 recall was linked to Day1-Day3 pattern dissimilarity in controls, suggesting the use of a different trace, whereas stressed participants relied on the original memory representation. These neural representation changes were again dependent on VTC reinstatement during reactivation. Together, our findings suggest that the impairing effects of post-retrieval stress on future memory relate to the strength of reactivation of the original memory trace, driven by the hippocampus and its crosstalk with neocortical representation areas, revealing disruptive effects on the formation of multiple memory traces

Causal role of the angular gyrus in insight-driven memory reconfiguration - restricted

Maintaining an accurate model of the world relies on our ability to update memory representations in light of new information. Previous research on the integration of new information into memory mainly focused on the hippocampus. Here, we hypothesized that the angular gyrus, known to be involved in episodic memory and imagination, plays a pivotal role in the insight-driven reconfiguration of memory representations. To test this hypothesis, participants received continuous theta burst stimulation (cTBS) inhibiting the left angular gyrus or sham stimulation before gaining insight into the relationship between previously separate life-like animated events in a narrative-insight task. During this task, participants also underwent EEG recording and their memory for linked and non-linked events was assessed shortly thereafter. Our results show that cTBS to the angular gyrus decreased memory for the linking events and reduced the memory advantage for linked relative to non-linked events. At the neural level, cTBS-induced angular gyrus inhibition reduced centro-temporal coupling with frontal regions and abolished insight-induced neural representational changes for events linked via imagination, indicating impaired memory reconfiguration. Further, the cTBS group showed representational changes for non-linked events that resembled the patterns observed in the sham group for the linked events, suggesting failed pruning of the narrative in memory. Together, our findings demonstrate a causal role of the left angular gyrus in insight-related memory reconfigurations

Causal role of the angular gyrus in insight-driven memory reconfiguration

Maintaining an accurate model of the world relies on our ability to update memory representations in light of new information. Previous research on the integration of new information into memory mainly focused on the hippocampus. Here, we hypothesized that the angular gyrus, known to be involved in episodic memory and imagination, plays a pivotal role in the insight-driven reconfiguration of memory representations. To test this hypothesis, participants received continuous theta burst stimulation (cTBS) inhibiting the left angular gyrus or sham stimulation before gaining insight into the relationship between previously separate life-like animated events in a narrative-insight task. During this task, participants also underwent EEG recording and their memory for linked and non-linked events was assessed shortly thereafter. Our results show that cTBS to the angular gyrus decreased memory for the linking events and reduced the memory advantage for linked relative to non-linked events. At the neural level, cTBS-induced angular gyrus inhibition reduced centro-temporal coupling with frontal regions and abolished insight-induced neural representational changes for events linked via imagination, indicating impaired memory reconfiguration. Further, the cTBS group showed representational changes for non-linked events that resembled the patterns observed in the sham group for the linked events, suggesting failed pruning of the narrative in memory. Together, our findings demonstrate a causal role of the left angular gyrus in insight-related memory reconfigurations

Causal role of the angular gyrus in insight-driven memory reconfiguration

Maintaining an accurate model of the world relies on our ability to update memory representations in light of new information. Previous research on the integration of new information into memory mainly focused on the hippocampus. Here, we hypothesized that the angular gyrus, known to be involved in episodic memory and imagination, plays a pivotal role in the insight-driven reconfiguration of memory representations. To test this hypothesis, participants received continuous theta burst stimulation (cTBS) over the left angular gyrus or sham stimulation before gaining insight into the relationship between previously separate life-like animated events in a narrative-insight task. During this task, participants also underwent EEG recording and their memory for linked and non-linked events was assessed shortly thereafter. Our results show that cTBS to the angular gyrus decreased memory for the linking events and reduced the memory advantage for linked relative to non-linked events. At the neural level, cTBS targeting the angular gyrus reduced centro-temporal coupling with frontal regions and abolished insight-induced neural representational changes for events linked via imagination, indicating impaired memory reconfiguration. Further, the cTBS group showed representational changes for non-linked events that resembled the patterns observed in the sham group for the linked events, suggesting failed pruning of the narrative in memory. Together, our findings demonstrate a causal role of the left angular gyrus in insight-related memory reconfigurations

Stress enhances emotional memory-related theta oscillations in the medial temporal lobe

Stressful events impact memory formation, in particular for emotionally arousing stimuli. Although these stress effects on emotional memory formation have potentially far-reaching implications, the underlying neural mechanisms are not fully understood. Specifically, the temporal processing dimension of the mechanisms involved in emotional memory formation under stress remains elusive. Here, we used magnetoencephalography (MEG) to examine the neural processes underlying stress effects on emotional memory formation with high temporal and spatial resolution and a particular focus on theta oscillations previously implicated in mnemonic binding. Healthy participants (n = 53) underwent a stress or control procedure before encoding emotionally neutral and negative pictures, while MEG was recorded. Memory for the pictures was probed in a recognition test 24 h after encoding. In this recognition test, stress did not modulate the emotional memory enhancement but led to significantly higher confidence in memory for negative compared to neutral stimuli. Our neural data revealed that stress increased memory-related theta oscillations specifically in medial temporal and occipito-parietal regions. Further, this stress-related increase in theta power emerged during memory formation for emotionally negative but not for neutral stimuli. These findings indicate that acute stress can enhance, in the medial temporal lobe, oscillations at a frequency that is ideally suited to bind the elements of an ongoing emotional episode, which may represent a mechanism to facilitate the storage of emotionally salient events that occurred in the context of a stressful encounter