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Interventions after acute stress prevent its delayed effects on the amygdala

Stress is known to elicit contrasting patterns of plasticity in the amygdala and hippocampus. While chronic stress leads to neuronal atrophy in the rodent hippocampus, it has the opposite effect in the basolateral amygdala (BLA). Further, even a single episode of acute stress is known to elicit dela...

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Autores principales: Chakraborty, Prabahan, Chattarji, Sumantra
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6535648/
https://www.ncbi.nlm.nih.gov/pubmed/31193585
http://dx.doi.org/10.1016/j.ynstr.2019.100168
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author Chakraborty, Prabahan
Chattarji, Sumantra
author_facet Chakraborty, Prabahan
Chattarji, Sumantra
author_sort Chakraborty, Prabahan
collection PubMed
description Stress is known to elicit contrasting patterns of plasticity in the amygdala and hippocampus. While chronic stress leads to neuronal atrophy in the rodent hippocampus, it has the opposite effect in the basolateral amygdala (BLA). Further, even a single episode of acute stress is known to elicit delayed effects in the amygdala. For example, 2 h of immobilisation stress has been shown to cause a delayed increase in dendritic spine density on BLA principal neurons 10 days later in young rats. This is paralleled by higher anxiety-like behaviour at the same delayed time point. This temporal build-up of morphological and behavioural effects 10 days later, in turn, provides a stress-free time window of intervention after exposure to acute stress. Here, we explore this possibility by specifically testing the efficacy of an anxiolytic drug in reversing the delayed effects of acute immobilisation stress. Oral gavage of diazepam 1 h after immobilisation stress prevented the increase in anxiety-like behaviour on the elevated plus-maze 10 days later. The same post-stress intervention also prevented delayed spinogenesis in the BLA 10 days after acute stress. Surprisingly, gavage of only the vehicle also had a protective effect on both the behavioural and synaptic effects of stress 10 days later. Vehicle gavage was found to trigger a significant rise in corticosterone levels that was comparable to that elicited by acute stress. This suggests that a surge in corticosterone levels, caused by the vehicle gavage 1 h after acute stress, was capable of reversing the delayed enhancing effects of stress on anxiety-like behaviour and BLA synaptic connectivity. These findings are consistent with clinical reports on the protective effects of glucocorticoids against the development of symptoms of post-traumatic stress disorder. Taken together, these results reveal strategies, targeted 1 h after stress, which can prevent the delayed effects of a brief exposure to a severe physical stressor.
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spelling pubmed-65356482019-05-30 Interventions after acute stress prevent its delayed effects on the amygdala Chakraborty, Prabahan Chattarji, Sumantra Neurobiol Stress Article from the Special Issue on Stress Neurobiology Workshop 2018; Edited by Lawrence Reagan,Richard Hunter and Matthew N. Hill Stress is known to elicit contrasting patterns of plasticity in the amygdala and hippocampus. While chronic stress leads to neuronal atrophy in the rodent hippocampus, it has the opposite effect in the basolateral amygdala (BLA). Further, even a single episode of acute stress is known to elicit delayed effects in the amygdala. For example, 2 h of immobilisation stress has been shown to cause a delayed increase in dendritic spine density on BLA principal neurons 10 days later in young rats. This is paralleled by higher anxiety-like behaviour at the same delayed time point. This temporal build-up of morphological and behavioural effects 10 days later, in turn, provides a stress-free time window of intervention after exposure to acute stress. Here, we explore this possibility by specifically testing the efficacy of an anxiolytic drug in reversing the delayed effects of acute immobilisation stress. Oral gavage of diazepam 1 h after immobilisation stress prevented the increase in anxiety-like behaviour on the elevated plus-maze 10 days later. The same post-stress intervention also prevented delayed spinogenesis in the BLA 10 days after acute stress. Surprisingly, gavage of only the vehicle also had a protective effect on both the behavioural and synaptic effects of stress 10 days later. Vehicle gavage was found to trigger a significant rise in corticosterone levels that was comparable to that elicited by acute stress. This suggests that a surge in corticosterone levels, caused by the vehicle gavage 1 h after acute stress, was capable of reversing the delayed enhancing effects of stress on anxiety-like behaviour and BLA synaptic connectivity. These findings are consistent with clinical reports on the protective effects of glucocorticoids against the development of symptoms of post-traumatic stress disorder. Taken together, these results reveal strategies, targeted 1 h after stress, which can prevent the delayed effects of a brief exposure to a severe physical stressor. Elsevier 2019-04-30 /pmc/articles/PMC6535648/ /pubmed/31193585 http://dx.doi.org/10.1016/j.ynstr.2019.100168 Text en © 2019 The Authors http://creativecommons.org/licenses/by/4.0/ This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Article from the Special Issue on Stress Neurobiology Workshop 2018; Edited by Lawrence Reagan,Richard Hunter and Matthew N. Hill
Chakraborty, Prabahan
Chattarji, Sumantra
Interventions after acute stress prevent its delayed effects on the amygdala
title Interventions after acute stress prevent its delayed effects on the amygdala
title_full Interventions after acute stress prevent its delayed effects on the amygdala
title_fullStr Interventions after acute stress prevent its delayed effects on the amygdala
title_full_unstemmed Interventions after acute stress prevent its delayed effects on the amygdala
title_short Interventions after acute stress prevent its delayed effects on the amygdala
title_sort interventions after acute stress prevent its delayed effects on the amygdala
topic Article from the Special Issue on Stress Neurobiology Workshop 2018; Edited by Lawrence Reagan,Richard Hunter and Matthew N. Hill
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6535648/
https://www.ncbi.nlm.nih.gov/pubmed/31193585
http://dx.doi.org/10.1016/j.ynstr.2019.100168
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