Stress-Induced Memory Retrieval Impairments: Different Time-Course Involvement of Corticosterone and Glucocorticoid Receptors in Dorsal and Ventral Hippocampus

The present study was aimed at determining the relative contribution of the dorsal (DH) and ventral (VH) hippocampus in stress-induced memory retrieval impairments. Thus, we studied the temporal involvement of corticosterone and its receptors, i.e. mineralocorticoid (MR) and glucocorticoid (GR) in t...

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Main Authors: Dorey, R, Piérard, C, Chauveau, F, David, V, Béracochéa, D
Format: Online
Language:English
Published: Nature Publishing Group 2012
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3499833/
id pubmed-3499833
recordtype oai_dc
spelling pubmed-34998332012-12-01 Stress-Induced Memory Retrieval Impairments: Different Time-Course Involvement of Corticosterone and Glucocorticoid Receptors in Dorsal and Ventral Hippocampus Dorey, R Piérard, C Chauveau, F David, V Béracochéa, D Original Article The present study was aimed at determining the relative contribution of the dorsal (DH) and ventral (VH) hippocampus in stress-induced memory retrieval impairments. Thus, we studied the temporal involvement of corticosterone and its receptors, i.e. mineralocorticoid (MR) and glucocorticoid (GR) in the DH and VH, in relation with the time-course evolution of stress-induced memory retrieval impairments. In a first experiment, double microdialysis allowed showing on the same animal that an acute stress (electric footshocks) induced an earlier corticosterone rise in the DH (15–60 min post-stress) and then in the VH (90–105 min post-stress). The return to baseline was faster in the DH (105 min) than in the VH (120 min). Memory deficits assessed by delayed alternation occurred at 15-, 60-, and 105-min delays after stress and were closely related to the kinetic of corticosterone rises within the DH and VH. In a second experiment, the GR antagonist RU-38486 and the MR antagonist RU-28318 were administered in the DH or VH 15 min before stress. RU-38486 restored memory at 60 but not at 105 min post-stress delays in the DH, whereas the opposite pattern was observed in the VH. By contrast, RU-28318 had no effect on memory impairments at both the 60- and 105-min post-stress delays, showing that MR receptors are not involved at these delays. However, RU-28318 administered in the DH restored memory when administered at a shorter post-stress delay (15 min). Overall, our data are first to evidence that stress induces a functional switch from the DH to VH via different corticosterone time-course evolutions in these areas and the sequential GR receptors involvement in the DH and then in the VH, as regards the persistence of stress-induced memory retrieval deficits over time. Nature Publishing Group 2012-12 2012-09-05 /pmc/articles/PMC3499833/ /pubmed/22948976 http://dx.doi.org/10.1038/npp.2012.170 Text en Copyright © 2012 American College of Neuropsychopharmacology http://creativecommons.org/licenses/by-nc-nd/3.0/ This work is licensed under the Creative Commons Attribution-NonCommercial-No Derivative Works 3.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-nd/3.0/
repository_type Open Access Journal
institution_category Foreign Institution
institution US National Center for Biotechnology Information
building NCBI PubMed
collection Online Access
language English
format Online
author Dorey, R
Piérard, C
Chauveau, F
David, V
Béracochéa, D
spellingShingle Dorey, R
Piérard, C
Chauveau, F
David, V
Béracochéa, D
Stress-Induced Memory Retrieval Impairments: Different Time-Course Involvement of Corticosterone and Glucocorticoid Receptors in Dorsal and Ventral Hippocampus
author_facet Dorey, R
Piérard, C
Chauveau, F
David, V
Béracochéa, D
author_sort Dorey, R
title Stress-Induced Memory Retrieval Impairments: Different Time-Course Involvement of Corticosterone and Glucocorticoid Receptors in Dorsal and Ventral Hippocampus
title_short Stress-Induced Memory Retrieval Impairments: Different Time-Course Involvement of Corticosterone and Glucocorticoid Receptors in Dorsal and Ventral Hippocampus
title_full Stress-Induced Memory Retrieval Impairments: Different Time-Course Involvement of Corticosterone and Glucocorticoid Receptors in Dorsal and Ventral Hippocampus
title_fullStr Stress-Induced Memory Retrieval Impairments: Different Time-Course Involvement of Corticosterone and Glucocorticoid Receptors in Dorsal and Ventral Hippocampus
title_full_unstemmed Stress-Induced Memory Retrieval Impairments: Different Time-Course Involvement of Corticosterone and Glucocorticoid Receptors in Dorsal and Ventral Hippocampus
title_sort stress-induced memory retrieval impairments: different time-course involvement of corticosterone and glucocorticoid receptors in dorsal and ventral hippocampus
description The present study was aimed at determining the relative contribution of the dorsal (DH) and ventral (VH) hippocampus in stress-induced memory retrieval impairments. Thus, we studied the temporal involvement of corticosterone and its receptors, i.e. mineralocorticoid (MR) and glucocorticoid (GR) in the DH and VH, in relation with the time-course evolution of stress-induced memory retrieval impairments. In a first experiment, double microdialysis allowed showing on the same animal that an acute stress (electric footshocks) induced an earlier corticosterone rise in the DH (15–60 min post-stress) and then in the VH (90–105 min post-stress). The return to baseline was faster in the DH (105 min) than in the VH (120 min). Memory deficits assessed by delayed alternation occurred at 15-, 60-, and 105-min delays after stress and were closely related to the kinetic of corticosterone rises within the DH and VH. In a second experiment, the GR antagonist RU-38486 and the MR antagonist RU-28318 were administered in the DH or VH 15 min before stress. RU-38486 restored memory at 60 but not at 105 min post-stress delays in the DH, whereas the opposite pattern was observed in the VH. By contrast, RU-28318 had no effect on memory impairments at both the 60- and 105-min post-stress delays, showing that MR receptors are not involved at these delays. However, RU-28318 administered in the DH restored memory when administered at a shorter post-stress delay (15 min). Overall, our data are first to evidence that stress induces a functional switch from the DH to VH via different corticosterone time-course evolutions in these areas and the sequential GR receptors involvement in the DH and then in the VH, as regards the persistence of stress-induced memory retrieval deficits over time.
publisher Nature Publishing Group
publishDate 2012
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3499833/
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