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Neural correlates of sleep‐induced benefits on traumatic memory processing

Recent findings indicate that sleep after trauma compared to sleep loss inhibits intrusive memory development, possibly by promoting adequate memory consolidation and integration. However, the underlying neural mechanisms are still unknown. Here, we examined the neural correlates underlying the effe...

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Autores principales: Gvozdanovic, Geraldine, Schoch, Sarah, Stämpfli, Philipp, Seifritz, Erich, Rasch, Björn
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley & Sons, Inc. 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10203801/
https://www.ncbi.nlm.nih.gov/pubmed/36999915
http://dx.doi.org/10.1002/hbm.26294
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author Gvozdanovic, Geraldine
Schoch, Sarah
Stämpfli, Philipp
Seifritz, Erich
Rasch, Björn
author_facet Gvozdanovic, Geraldine
Schoch, Sarah
Stämpfli, Philipp
Seifritz, Erich
Rasch, Björn
author_sort Gvozdanovic, Geraldine
collection PubMed
description Recent findings indicate that sleep after trauma compared to sleep loss inhibits intrusive memory development, possibly by promoting adequate memory consolidation and integration. However, the underlying neural mechanisms are still unknown. Here, we examined the neural correlates underlying the effects of sleep on traumatic memory development in 110 healthy participants using a trauma film paradigm and an implicit memory task with fMRI recordings in a between‐subjects design. To further facilitate memory integration, we used targeted memory reactivation (TMR) to reactivate traumatic memories during sleep. We found that sleep (i.e., nap) compared to wakefulness reduced the number of intrusive traumatic memories for the experimental trauma groups. TMR during sleep only descriptively reduced the intrusions further. On the level of brain activity, increased activity in the anterior and posterior cingulate cortex, retrosplenial cortex and precuneus was found in the experimental trauma group compared to the control group after wakefulness. After sleep, on the other hand, these findings could not be found in the experimental trauma groups compared to the control group. Sleep compared to wakefulness increased activity in the cerebellum, fusiform gyrus, inferior temporal lobe, hippocampus, and amygdala during implicit retrieval of trauma memories in the experimental trauma groups. Activity in the hippocampus and the amygdala predicted subsequent intrusions. Results demonstrate the beneficial behavioral and neural effects of sleep after experimental trauma and provide indications for early neural predictor factors. This study has implications for understanding the important role of sleep for personalized treatment and prevention in posttraumatic stress disorder.
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spelling pubmed-102038012023-05-24 Neural correlates of sleep‐induced benefits on traumatic memory processing Gvozdanovic, Geraldine Schoch, Sarah Stämpfli, Philipp Seifritz, Erich Rasch, Björn Hum Brain Mapp Research Articles Recent findings indicate that sleep after trauma compared to sleep loss inhibits intrusive memory development, possibly by promoting adequate memory consolidation and integration. However, the underlying neural mechanisms are still unknown. Here, we examined the neural correlates underlying the effects of sleep on traumatic memory development in 110 healthy participants using a trauma film paradigm and an implicit memory task with fMRI recordings in a between‐subjects design. To further facilitate memory integration, we used targeted memory reactivation (TMR) to reactivate traumatic memories during sleep. We found that sleep (i.e., nap) compared to wakefulness reduced the number of intrusive traumatic memories for the experimental trauma groups. TMR during sleep only descriptively reduced the intrusions further. On the level of brain activity, increased activity in the anterior and posterior cingulate cortex, retrosplenial cortex and precuneus was found in the experimental trauma group compared to the control group after wakefulness. After sleep, on the other hand, these findings could not be found in the experimental trauma groups compared to the control group. Sleep compared to wakefulness increased activity in the cerebellum, fusiform gyrus, inferior temporal lobe, hippocampus, and amygdala during implicit retrieval of trauma memories in the experimental trauma groups. Activity in the hippocampus and the amygdala predicted subsequent intrusions. Results demonstrate the beneficial behavioral and neural effects of sleep after experimental trauma and provide indications for early neural predictor factors. This study has implications for understanding the important role of sleep for personalized treatment and prevention in posttraumatic stress disorder. John Wiley & Sons, Inc. 2023-03-31 /pmc/articles/PMC10203801/ /pubmed/36999915 http://dx.doi.org/10.1002/hbm.26294 Text en © 2023 The Authors. Human Brain Mapping published by Wiley Periodicals LLC. https://creativecommons.org/licenses/by-nc/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc/4.0/ (https://creativecommons.org/licenses/by-nc/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.
spellingShingle Research Articles
Gvozdanovic, Geraldine
Schoch, Sarah
Stämpfli, Philipp
Seifritz, Erich
Rasch, Björn
Neural correlates of sleep‐induced benefits on traumatic memory processing
title Neural correlates of sleep‐induced benefits on traumatic memory processing
title_full Neural correlates of sleep‐induced benefits on traumatic memory processing
title_fullStr Neural correlates of sleep‐induced benefits on traumatic memory processing
title_full_unstemmed Neural correlates of sleep‐induced benefits on traumatic memory processing
title_short Neural correlates of sleep‐induced benefits on traumatic memory processing
title_sort neural correlates of sleep‐induced benefits on traumatic memory processing
topic Research Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10203801/
https://www.ncbi.nlm.nih.gov/pubmed/36999915
http://dx.doi.org/10.1002/hbm.26294
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