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Contributions of glucocorticoid receptors in cortical astrocytes to memory recall
Dysfunctions in memory recall lead to pathological fear; a hallmark of trauma-related disorders, like posttraumatic stress disorder (PTSD). Both, heightened recall of an association between a cue and trauma, as well as impoverished recall that a previously trauma-related cue is no longer a threat, r...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Cold Spring Harbor Laboratory Press
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7970741/ https://www.ncbi.nlm.nih.gov/pubmed/33723032 http://dx.doi.org/10.1101/lm.053041.120 |
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author | Taylor, William W. Imhoff, Barry R. Sathi, Zakia Sultana Liu, Wei Y. Garza, Kristie M. Dias, Brian G. |
author_facet | Taylor, William W. Imhoff, Barry R. Sathi, Zakia Sultana Liu, Wei Y. Garza, Kristie M. Dias, Brian G. |
author_sort | Taylor, William W. |
collection | PubMed |
description | Dysfunctions in memory recall lead to pathological fear; a hallmark of trauma-related disorders, like posttraumatic stress disorder (PTSD). Both, heightened recall of an association between a cue and trauma, as well as impoverished recall that a previously trauma-related cue is no longer a threat, result in a debilitating fear toward the cue. Glucocorticoid-mediated action via the glucocorticoid receptor (GR) influences memory recall. This literature has primarily focused on GRs expressed in neurons or ignored cell-type specific contributions. To ask how GR action in nonneuronal cells influences memory recall, we combined auditory fear conditioning in mice and the knockout of GRs in astrocytes in the prefrontal cortex (PFC), a brain region implicated in memory recall. We found that knocking out GRs in astrocytes of the PFC disrupted memory recall. Specifically, we found that knocking out GRs in astrocytes in the PFC (AstroGRKO) after fear conditioning resulted in higher levels of freezing to the CS+ tone when compared with controls (AstroGRintact). While we did not find any differences in extinction of fear toward the CS+ between these groups, AstroGRKO female but not male mice showed impaired recall of extinction training. These results suggest that GRs in cortical astrocytes contribute to memory recall. These data demonstrate the need to examine GR action in cortical astrocytes to elucidate the basic neurobiology underlying memory recall and potential mechanisms that underlie female-specific biases in the incidence of PTSD. |
format | Online Article Text |
id | pubmed-7970741 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Cold Spring Harbor Laboratory Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-79707412021-04-01 Contributions of glucocorticoid receptors in cortical astrocytes to memory recall Taylor, William W. Imhoff, Barry R. Sathi, Zakia Sultana Liu, Wei Y. Garza, Kristie M. Dias, Brian G. Learn Mem Research Dysfunctions in memory recall lead to pathological fear; a hallmark of trauma-related disorders, like posttraumatic stress disorder (PTSD). Both, heightened recall of an association between a cue and trauma, as well as impoverished recall that a previously trauma-related cue is no longer a threat, result in a debilitating fear toward the cue. Glucocorticoid-mediated action via the glucocorticoid receptor (GR) influences memory recall. This literature has primarily focused on GRs expressed in neurons or ignored cell-type specific contributions. To ask how GR action in nonneuronal cells influences memory recall, we combined auditory fear conditioning in mice and the knockout of GRs in astrocytes in the prefrontal cortex (PFC), a brain region implicated in memory recall. We found that knocking out GRs in astrocytes of the PFC disrupted memory recall. Specifically, we found that knocking out GRs in astrocytes in the PFC (AstroGRKO) after fear conditioning resulted in higher levels of freezing to the CS+ tone when compared with controls (AstroGRintact). While we did not find any differences in extinction of fear toward the CS+ between these groups, AstroGRKO female but not male mice showed impaired recall of extinction training. These results suggest that GRs in cortical astrocytes contribute to memory recall. These data demonstrate the need to examine GR action in cortical astrocytes to elucidate the basic neurobiology underlying memory recall and potential mechanisms that underlie female-specific biases in the incidence of PTSD. Cold Spring Harbor Laboratory Press 2021-04 /pmc/articles/PMC7970741/ /pubmed/33723032 http://dx.doi.org/10.1101/lm.053041.120 Text en © 2021 Taylor et al.; Published by Cold Spring Harbor Laboratory Press http://creativecommons.org/licenses/by/4.0/ This article, published in Learning & Memory, is available under a Creative Commons License (Attribution 4.0 International), as described at http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Research Taylor, William W. Imhoff, Barry R. Sathi, Zakia Sultana Liu, Wei Y. Garza, Kristie M. Dias, Brian G. Contributions of glucocorticoid receptors in cortical astrocytes to memory recall |
title | Contributions of glucocorticoid receptors in cortical astrocytes to memory recall |
title_full | Contributions of glucocorticoid receptors in cortical astrocytes to memory recall |
title_fullStr | Contributions of glucocorticoid receptors in cortical astrocytes to memory recall |
title_full_unstemmed | Contributions of glucocorticoid receptors in cortical astrocytes to memory recall |
title_short | Contributions of glucocorticoid receptors in cortical astrocytes to memory recall |
title_sort | contributions of glucocorticoid receptors in cortical astrocytes to memory recall |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7970741/ https://www.ncbi.nlm.nih.gov/pubmed/33723032 http://dx.doi.org/10.1101/lm.053041.120 |
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