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Extended amygdala connectivity changes during sustained shock anticipation
The bed nucleus of the stria terminalis (BNST) and central amygdala (CeA) of the extended amygdala are small, anatomically interconnected brain regions. They are thought to mediate responses to sustained, unpredictable threat stimuli and phasic, predictable threat stimuli, respectively. They perform...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5802685/ https://www.ncbi.nlm.nih.gov/pubmed/29382815 http://dx.doi.org/10.1038/s41398-017-0074-6 |
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author | Torrisi, Salvatore Gorka, Adam X. Gonzalez-Castillo, Javier O’Connell, Katherine Balderston, Nicholas Grillon, Christian Ernst, Monique |
author_facet | Torrisi, Salvatore Gorka, Adam X. Gonzalez-Castillo, Javier O’Connell, Katherine Balderston, Nicholas Grillon, Christian Ernst, Monique |
author_sort | Torrisi, Salvatore |
collection | PubMed |
description | The bed nucleus of the stria terminalis (BNST) and central amygdala (CeA) of the extended amygdala are small, anatomically interconnected brain regions. They are thought to mediate responses to sustained, unpredictable threat stimuli and phasic, predictable threat stimuli, respectively. They perform these operations largely through their interconnected networks. In two previous studies, we mapped and contrasted the resting functional connectivity networks of the BNST and CeA at 7 Tesla with high resolution. This follow-up study investigates the changes in functional connectivity of these structures during sustained anticipation of electric shock. Results show that the BNST and CeA become less strongly coupled with the ventromedial prefrontal cortex (vmPFC), cingulate, and nucleus accumbens in shock threat relative to a safety condition. In addition, the CeA becomes more strongly coupled with the thalamus under threat. An exploratory, whole-brain connectivity analysis reveals that, although the BNST/CeA exhibits generally decreased connectivity, many other cortical regions demonstrate greater coupling under threat than safety. Understanding the differential network structures of these two regions and how they contribute to processing under threat will help elucidate the building blocks of the anxious state. |
format | Online Article Text |
id | pubmed-5802685 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-58026852018-02-08 Extended amygdala connectivity changes during sustained shock anticipation Torrisi, Salvatore Gorka, Adam X. Gonzalez-Castillo, Javier O’Connell, Katherine Balderston, Nicholas Grillon, Christian Ernst, Monique Transl Psychiatry Review Article The bed nucleus of the stria terminalis (BNST) and central amygdala (CeA) of the extended amygdala are small, anatomically interconnected brain regions. They are thought to mediate responses to sustained, unpredictable threat stimuli and phasic, predictable threat stimuli, respectively. They perform these operations largely through their interconnected networks. In two previous studies, we mapped and contrasted the resting functional connectivity networks of the BNST and CeA at 7 Tesla with high resolution. This follow-up study investigates the changes in functional connectivity of these structures during sustained anticipation of electric shock. Results show that the BNST and CeA become less strongly coupled with the ventromedial prefrontal cortex (vmPFC), cingulate, and nucleus accumbens in shock threat relative to a safety condition. In addition, the CeA becomes more strongly coupled with the thalamus under threat. An exploratory, whole-brain connectivity analysis reveals that, although the BNST/CeA exhibits generally decreased connectivity, many other cortical regions demonstrate greater coupling under threat than safety. Understanding the differential network structures of these two regions and how they contribute to processing under threat will help elucidate the building blocks of the anxious state. Nature Publishing Group UK 2018-01-31 /pmc/articles/PMC5802685/ /pubmed/29382815 http://dx.doi.org/10.1038/s41398-017-0074-6 Text en © The Author(s) 2018 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Review Article Torrisi, Salvatore Gorka, Adam X. Gonzalez-Castillo, Javier O’Connell, Katherine Balderston, Nicholas Grillon, Christian Ernst, Monique Extended amygdala connectivity changes during sustained shock anticipation |
title | Extended amygdala connectivity changes during sustained shock anticipation |
title_full | Extended amygdala connectivity changes during sustained shock anticipation |
title_fullStr | Extended amygdala connectivity changes during sustained shock anticipation |
title_full_unstemmed | Extended amygdala connectivity changes during sustained shock anticipation |
title_short | Extended amygdala connectivity changes during sustained shock anticipation |
title_sort | extended amygdala connectivity changes during sustained shock anticipation |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5802685/ https://www.ncbi.nlm.nih.gov/pubmed/29382815 http://dx.doi.org/10.1038/s41398-017-0074-6 |
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