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Intact Recognition Memory and Altered Hippocampal Glucocorticoid Receptor Signaling in Fkbp5-deficient Mice Following Acute Uncontrollable Stress

The FK506 binding protein 5 (FKBP5) is a co-chaperone that regulates the activity of the glucocorticoid receptor (GR) and has been reported to mediate stress resilience. This study aimed to determine the effects of Fkbp5 deletion on acute stress-induced recognition memory impairment and hippocampal...

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Autores principales: Jeon, Yong-Jae, Choi, Bo-Ryoung, Park, Min-Sun, Jang, Yoon-Sun, Yoon, Sujung, Lyoo, In Kyoon, Han, Jung-Soo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Korean Society for Brain and Neural Sciences 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10175958/
https://www.ncbi.nlm.nih.gov/pubmed/37164649
http://dx.doi.org/10.5607/en23006
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author Jeon, Yong-Jae
Choi, Bo-Ryoung
Park, Min-Sun
Jang, Yoon-Sun
Yoon, Sujung
Lyoo, In Kyoon
Han, Jung-Soo
author_facet Jeon, Yong-Jae
Choi, Bo-Ryoung
Park, Min-Sun
Jang, Yoon-Sun
Yoon, Sujung
Lyoo, In Kyoon
Han, Jung-Soo
author_sort Jeon, Yong-Jae
collection PubMed
description The FK506 binding protein 5 (FKBP5) is a co-chaperone that regulates the activity of the glucocorticoid receptor (GR) and has been reported to mediate stress resilience. This study aimed to determine the effects of Fkbp5 deletion on acute stress-induced recognition memory impairment and hippocampal GR signaling. Wild-type and Fkbp5-knockout mice were subjected to acute uncontrollable stress induced by restraint and electrical tail shock. First, we assessed the cognitive status of mice using a novel object recognition task. Next, we measured plasma corticosterone, GR levels, and the levels of GR phosphorylation at serine 211 in the hippocampus. Wild-type mice exhibited stress-induced memory impairments, whereas Fkbp5-knockout mice did not. Plasma corticosterone and GR levels did not differ between the non-stressed wild-type and Fkbp5-knockout mice, but the levels of phosphorylated GR were lower in Fkbp5-knockout mice than in wild-type mice. Wild-type and Fkbp5-knockout mice showed increased nuclear GR levels following stress, indicating GR translocation. However, cytosolic phosphorylated GR levels were lower in the hippocampi of Fkbp5-knockout mice following stress than in those of wild-type mice. These results suggest that FKBP5 deficiency increases resilience to acute stress by altering GR signaling.
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spelling pubmed-101759582023-05-13 Intact Recognition Memory and Altered Hippocampal Glucocorticoid Receptor Signaling in Fkbp5-deficient Mice Following Acute Uncontrollable Stress Jeon, Yong-Jae Choi, Bo-Ryoung Park, Min-Sun Jang, Yoon-Sun Yoon, Sujung Lyoo, In Kyoon Han, Jung-Soo Exp Neurobiol Original Article The FK506 binding protein 5 (FKBP5) is a co-chaperone that regulates the activity of the glucocorticoid receptor (GR) and has been reported to mediate stress resilience. This study aimed to determine the effects of Fkbp5 deletion on acute stress-induced recognition memory impairment and hippocampal GR signaling. Wild-type and Fkbp5-knockout mice were subjected to acute uncontrollable stress induced by restraint and electrical tail shock. First, we assessed the cognitive status of mice using a novel object recognition task. Next, we measured plasma corticosterone, GR levels, and the levels of GR phosphorylation at serine 211 in the hippocampus. Wild-type mice exhibited stress-induced memory impairments, whereas Fkbp5-knockout mice did not. Plasma corticosterone and GR levels did not differ between the non-stressed wild-type and Fkbp5-knockout mice, but the levels of phosphorylated GR were lower in Fkbp5-knockout mice than in wild-type mice. Wild-type and Fkbp5-knockout mice showed increased nuclear GR levels following stress, indicating GR translocation. However, cytosolic phosphorylated GR levels were lower in the hippocampi of Fkbp5-knockout mice following stress than in those of wild-type mice. These results suggest that FKBP5 deficiency increases resilience to acute stress by altering GR signaling. The Korean Society for Brain and Neural Sciences 2023-04-30 2023-04-30 /pmc/articles/PMC10175958/ /pubmed/37164649 http://dx.doi.org/10.5607/en23006 Text en Copyright © Experimental Neurobiology 2023 https://creativecommons.org/licenses/by-nc/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0 (https://creativecommons.org/licenses/by-nc/4.0/) ) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Article
Jeon, Yong-Jae
Choi, Bo-Ryoung
Park, Min-Sun
Jang, Yoon-Sun
Yoon, Sujung
Lyoo, In Kyoon
Han, Jung-Soo
Intact Recognition Memory and Altered Hippocampal Glucocorticoid Receptor Signaling in Fkbp5-deficient Mice Following Acute Uncontrollable Stress
title Intact Recognition Memory and Altered Hippocampal Glucocorticoid Receptor Signaling in Fkbp5-deficient Mice Following Acute Uncontrollable Stress
title_full Intact Recognition Memory and Altered Hippocampal Glucocorticoid Receptor Signaling in Fkbp5-deficient Mice Following Acute Uncontrollable Stress
title_fullStr Intact Recognition Memory and Altered Hippocampal Glucocorticoid Receptor Signaling in Fkbp5-deficient Mice Following Acute Uncontrollable Stress
title_full_unstemmed Intact Recognition Memory and Altered Hippocampal Glucocorticoid Receptor Signaling in Fkbp5-deficient Mice Following Acute Uncontrollable Stress
title_short Intact Recognition Memory and Altered Hippocampal Glucocorticoid Receptor Signaling in Fkbp5-deficient Mice Following Acute Uncontrollable Stress
title_sort intact recognition memory and altered hippocampal glucocorticoid receptor signaling in fkbp5-deficient mice following acute uncontrollable stress
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10175958/
https://www.ncbi.nlm.nih.gov/pubmed/37164649
http://dx.doi.org/10.5607/en23006
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