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Effects of a True Prophylactic Treatment on Hippocampal and Amygdala Synaptic Plasticity and Gene Expression in a Rodent Chronic Stress Model of Social Defeat

Post-traumatic stress disorder (PTSD) is a complex stress-related disorder induced by exposure to traumatic stress that is characterized by symptoms of re-experiencing, avoidance, and hyper-arousal. While it is widely accepted that brain regions involved in emotional regulation and memory-e.g., the...

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Published in:International journal of molecular sciences 2023-07, Vol.24 (13), p.11193
Main Authors: Winzenried, Eric T, Everett, Anna C, Saito, Erin R, Miller, Roxanne M, Johnson, Taylor, Neal, Eliza, Boyce, Zachary, Smith, Calvin, Jensen, Chloe, Kimball, Spencer, Brantley, Adam, Melendez, Gabriel, Moffat, Devin, Davis, Erin, Aponik, Lyndsey, Crofts, Tyler, Dabney, Bryson, Edwards, Jeffrey G
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cited_by cdi_FETCH-LOGICAL-c549t-2b1b4af5c0e77d93bab2c65e6c8b4f92e923c6e495907b4d7ccb6c0b5f2383a13
cites cdi_FETCH-LOGICAL-c549t-2b1b4af5c0e77d93bab2c65e6c8b4f92e923c6e495907b4d7ccb6c0b5f2383a13
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container_issue 13
container_start_page 11193
container_title International journal of molecular sciences
container_volume 24
creator Winzenried, Eric T
Everett, Anna C
Saito, Erin R
Miller, Roxanne M
Johnson, Taylor
Neal, Eliza
Boyce, Zachary
Smith, Calvin
Jensen, Chloe
Kimball, Spencer
Brantley, Adam
Melendez, Gabriel
Moffat, Devin
Davis, Erin
Aponik, Lyndsey
Crofts, Tyler
Dabney, Bryson
Edwards, Jeffrey G
description Post-traumatic stress disorder (PTSD) is a complex stress-related disorder induced by exposure to traumatic stress that is characterized by symptoms of re-experiencing, avoidance, and hyper-arousal. While it is widely accepted that brain regions involved in emotional regulation and memory-e.g., the amygdala and hippocampus-are dysregulated in PTSD, the pathophysiology of the disorder is not well defined and therefore, pharmacological interventions are extremely limited. Because stress hormones norepinephrine and cortisol (corticosterone in rats) are heavily implicated in the disorder, we explored whether preemptively and systemically antagonizing β-adrenergic and glucocorticoid receptors with propranolol and mifepristone are sufficient to mitigate pathological changes in synaptic plasticity, gene expression, and anxiety induced by a modified social defeat (SD) stress protocol. Young adult, male Sprague Dawley rats were initially pre-screened for anxiety. The rats were then exposed to SD and chronic light stress to induce anxiety-like symptoms. Drug-treated rats were administered propranolol and mifepristone injections prior to and continuing throughout SD stress. Using competitive ELISAs on plasma, field electrophysiology at CA1 of the ventral hippocampus (VH) and the basolateral amygdala (BLA), quantitative RT-PCR, and behavior assays, we demonstrate that our SD stress increased anxiety-like behavior, elevated long-term potentiation (LTP) in the VH and BLA, and altered the expression of mineralocorticoid, glucocorticoid, and glutamate receptors. These measures largely reverted to control levels with the administration of propranolol and mifepristone. Our findings indicate that SD stress increases LTP in the VH and BLA and that prophylactic treatment with propranolol and mifepristone may have the potential in mitigating these and other stress-induced effects.
doi_str_mv 10.3390/ijms241311193
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While it is widely accepted that brain regions involved in emotional regulation and memory-e.g., the amygdala and hippocampus-are dysregulated in PTSD, the pathophysiology of the disorder is not well defined and therefore, pharmacological interventions are extremely limited. Because stress hormones norepinephrine and cortisol (corticosterone in rats) are heavily implicated in the disorder, we explored whether preemptively and systemically antagonizing β-adrenergic and glucocorticoid receptors with propranolol and mifepristone are sufficient to mitigate pathological changes in synaptic plasticity, gene expression, and anxiety induced by a modified social defeat (SD) stress protocol. Young adult, male Sprague Dawley rats were initially pre-screened for anxiety. The rats were then exposed to SD and chronic light stress to induce anxiety-like symptoms. Drug-treated rats were administered propranolol and mifepristone injections prior to and continuing throughout SD stress. Using competitive ELISAs on plasma, field electrophysiology at CA1 of the ventral hippocampus (VH) and the basolateral amygdala (BLA), quantitative RT-PCR, and behavior assays, we demonstrate that our SD stress increased anxiety-like behavior, elevated long-term potentiation (LTP) in the VH and BLA, and altered the expression of mineralocorticoid, glucocorticoid, and glutamate receptors. These measures largely reverted to control levels with the administration of propranolol and mifepristone. Our findings indicate that SD stress increases LTP in the VH and BLA and that prophylactic treatment with propranolol and mifepristone may have the potential in mitigating these and other stress-induced effects.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>37446371</pmid><doi>10.3390/ijms241311193</doi><orcidid>https://orcid.org/0000-0001-7298-1889</orcidid><orcidid>https://orcid.org/0000-0003-1649-4722</orcidid><orcidid>https://orcid.org/0000-0002-3174-0605</orcidid><orcidid>https://orcid.org/0009-0001-2787-5822</orcidid><orcidid>https://orcid.org/0000-0002-8987-3443</orcidid><orcidid>https://orcid.org/0000-0002-8862-6969</orcidid><orcidid>https://orcid.org/0000-0003-4603-0320</orcidid><orcidid>https://orcid.org/0000-0002-2881-0772</orcidid><oa>free_for_read</oa></addata></record>
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identifier ISSN: 1422-0067
ispartof International journal of molecular sciences, 2023-07, Vol.24 (13), p.11193
issn 1422-0067
1661-6596
1422-0067
language eng
recordid cdi_doaj_primary_oai_doaj_org_article_3937a283fe85467a8d2974abc826ea38
source PubMed Central; ProQuest Publicly Available Content database
subjects Adrenergic receptors
Amygdala
Amygdala - metabolism
Animals
Anxiety
Arousal
Behavior
Corticosterone
Disease prevention
Electrophysiology
Females
Gene Expression
Genes
Glucocorticoid receptors
Glucocorticoids
Glutamic acid receptors
Hippocampal plasticity
Hippocampus
Hippocampus - metabolism
Hormones
Long-term potentiation
LTP
Male
Males
Medicine, Preventive
Mental disorders
Mifepristone
Mifepristone - pharmacology
Neuronal Plasticity
Neurophysiology
Norepinephrine
Physiological aspects
Post traumatic stress disorder
Preventive health services
Propranolol
Propranolol - pharmacology
Propranolol hydrochloride
Psychological stress
PTSD
rat
Rats
Rats, Sprague-Dawley
Rodentia
Rodents
Social Defeat
Social interactions
Stress, Psychological - complications
Synaptic plasticity
Young adults
title Effects of a True Prophylactic Treatment on Hippocampal and Amygdala Synaptic Plasticity and Gene Expression in a Rodent Chronic Stress Model of Social Defeat
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