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Shared memories reveal shared structure in neural activity across individuals.

ABSTRACT: Our lives revolve around sharing experiences and memories with others. When different people recount the same events, how similar are their underlying neural representations? Participants viewed a 50-min movie, then verbally described the events during functional MRI, producing unguided detailed descriptions lasting up to 40 min. As each person spoke, event-specific spatial patterns were reinstated in default-network, medial-temporal, and high-level visual areas. Individual event patterns were both highly discriminable from one another and similar among people, suggesting consistent spatial organization. In many high-order areas, patterns were more similar between people recalling the same event than between recall and perception, indicating systematic reshaping of percept into memory. These results reveal the existence of a common spatial organization for memories in high-level cortical areas, where encoded information is largely abstracted beyond sensory constraints, and that neural patterns during perception are altered systematically across people into shared memory representations for real-life events.

SUBMITTER: Chen J

PROVIDER: S-EPMC5191958 | biostudies-literature | 2017 Jan

REPOSITORIES: biostudies-literature

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Shared memories reveal shared structure in neural activity across individuals.

Chen Janice J Leong Yuan Chang YC Honey Christopher J CJ Yong Chung H CH Norman Kenneth A KA Hasson Uri U

Nature neuroscience 20161205 1

Our lives revolve around sharing experiences and memories with others. When different people recount the same events, how similar are their underlying neural representations? Participants viewed a 50-min movie, then verbally described the events during functional MRI, producing unguided detailed descriptions lasting up to 40 min. As each person spoke, event-specific spatial patterns were reinstated in default-network, medial-temporal, and high-level visual areas. Individual event patterns were b ...[more]

PMID: 27918531

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Project description:Functional neuroimaging evidence suggests that there are differences in the neural correlates of episodic memory for laboratory stimuli (laboratory memory) and for events from one's own life (autobiographical memory). However, this evidence is scarce and often confounded with differences in memory testing procedures. Here, we directly compared the neural mechanisms underlying the search and recovery of autobiographical and laboratory memories while minimizing testing differences. Before scanning, participants completed a laboratory memory encoding task in which they studied four-word "chains" spread across three word pairs. During scanning, participants completed a laboratory memory retrieval task, in which they recalled the word chains, and an autobiographical memory retrieval task, in which they recalled specific personal events associated with word cues. Importantly, response times were similar in the two tasks, allowing for a direct comparison of the activation time courses. We found that during memory search (searching for the memory target), similar brain regions were activated during both the autobiographical and laboratory tasks, whereas during memory recovery (accessing the memory traces; i.e., ecphory), clear differences emerged: regions of the default mode network (DMN) were activated greater during autobiographical than laboratory memory, whereas the bilateral superior parietal lobules were activated greater during laboratory than autobiographical memory. Also, multivariate functional connectivity analyses revealed that regardless of memory stage, the DMN and ventral attention network exhibited a more integrated topology in the functional network underlying autobiographical (vs. laboratory) memory retrieval, whereas the fronto-parietal task control network exhibited a more integrated topology in the functional network underlying laboratory (vs. autobiographical) memory retrieval. These findings further characterize the shared and distinct neural components underlying autobiographical and laboratory memories, and suggest that differences in autobiographical vs. laboratory memory brain activation previously reported in the literature reflect memory recovery rather than search differences.

Project description:When an item is predicted in a particular context but the prediction is violated, memory for that item is weakened (Kim et al., 2014). Here, we explore what happens when such previously mispredicted items are later reencountered. According to prior neural network simulations, this sequence of events-misprediction and subsequent restudy-should lead to differentiation of the item's neural representation from the previous context (on which the misprediction was based). Specifically, misprediction weakens connections in the representation to features shared with the previous context and restudy allows new features to be incorporated into the representation that are not shared with the previous context. This cycle of misprediction and restudy should have the net effect of moving the item's neural representation away from the neural representation of the previous context. We tested this hypothesis using human fMRI by tracking changes in item-specific BOLD activity patterns in the hippocampus, a key structure for representing memories and generating predictions. In left CA2/3/DG, we found greater neural differentiation for items that were repeatedly mispredicted and restudied compared with items from a control condition that was identical except without misprediction. We also measured prediction strength in a trial-by-trial fashion and found that greater misprediction for an item led to more differentiation, further supporting our hypothesis. Therefore, the consequences of prediction error go beyond memory weakening. If the mispredicted item is restudied, the brain adaptively differentiates its memory representation to improve the accuracy of subsequent predictions and to shield it from further weakening.SIGNIFICANCE STATEMENT Competition between overlapping memories leads to weakening of nontarget memories over time, making it easier to access target memories. However, a nontarget memory in one context might become a target memory in another context. How do such memories get restrengthened without increasing competition again? Computational models suggest that the brain handles this by reducing neural connections to the previous context and adding connections to new features that were not part of the previous context. The result is neural differentiation away from the previous context. Here, we provide support for this theory, using fMRI to track neural representations of individual memories in the hippocampus and how they change based on learning.

Project description:BackgroundInvoluntary memories are a hallmark symptom of posttraumatic stress disorder (PTSD), but studies of the neural basis of involuntary memory retrieval in posttraumatic stress disorder (PTSD) are sparse. The study of the neural correlates of involuntary memories of stressful events in PTSD focuses on the voluntary retrieval of memories that are sometimes recalled as intrusive involuntary memories, not on involuntary retrieval while being scanned. Involuntary memory retrieval in controls has been shown to elicit activity in the parahippocampal gyrus, precuneus, inferior parietal cortex, and posterior midline regions. However, it is unknown whether involuntary memories are supported by the same mechanisms in PTSD. Because previous work has shown that both behavioral and neural responsivity is slowed in PTSD, we examined the spatiotemporal dynamics of the neural activity underlying negative and neutral involuntary memory retrieval.MethodsTwenty-one individuals with PTSD and 21 non-PTSD, trauma-exposed controls performed an involuntary memory task, while undergoing a functional magnetic resonance imaging scan. Environmental sounds served as cues for well-associated pictures of negative and neutral scenes. We used a finite impulse response model to analyze temporal differences between groups in neural responses.ResultsCompared with controls, participants with PTSD reported more involuntary memories, which were more emotional and more vivid, but which activated a similar network of regions. However, compared to controls, individuals with PTSD showed delayed neural responsivity in this network and increased vmPFC/ACC activity for negative > neutral stimuli.ConclusionsThe similarity between PTSD and controls in neural substrates underlying involuntary memories suggests that, unlike voluntary memories, involuntary memories elicit similar activity in regions critical for memory retrieval. Further, the delayed neural responsivity for involuntary memories in PTSD suggests that factors affecting cognition in PTSD, like increased fatigue, or avoidance behaviors could do so by delaying activity in regions necessary for cognitive processing. Finally, compared to neutral memories, negative involuntary memories elicit hyperactivity in the vmPFC, whereas the vmPFC is typically shown to be hypoactive in PTSD during voluntary memory retrieval. These patterns suggest that considering both the temporal dynamics of cognitive processes as well as involuntary cognitive processes would improve existing neurobiological models of PTSD.

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Shared memories reveal shared structure in neural activity across individuals.

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Shared memories reveal shared structure in neural activity across individuals.

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