Is PTSD-Phenotype Associated with HPA-Axis Sensitivity? Feedback Inhibition and Other Modulating Factors of Glucocorticoid Signaling Dynamics

Previously, we found that basal corticosterone pulsatility significantly impacts the vulnerability for developing post-traumatic stress disorder (PTSD). Rats that exhibited PTSD-phenotype were characterized by blunted basal corticosterone pulsatility amplitude and a blunted corticosterone response t...

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Published inInternational journal of molecular sciences Vol. 22; no. 11; p. 6050
Main Authors Danan, Dor, Todder, Doron, Zohar, Joseph, Cohen, Hagit
Format Journal Article
LanguageEnglish
Published MDPI 03.06.2021
MDPI AG
Subjects
animal model
corticosterone
glucocorticoid receptor
hypothalamus–pituitary–adrenal axis
posttraumatic stress disorder
pulsatility
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Abstract Previously, we found that basal corticosterone pulsatility significantly impacts the vulnerability for developing post-traumatic stress disorder (PTSD). Rats that exhibited PTSD-phenotype were characterized by blunted basal corticosterone pulsatility amplitude and a blunted corticosterone response to a stressor. This study sought to identify the mechanisms underlining both the loss of pulsatility and differences in downstream responses. Serial blood samples were collected manually via jugular vein cannula at 10-min intervals to evaluate suppression of corticosterone following methylprednisolone administration. The rats were exposed to predator scent stress (PSS) after 24 h, and behavioral responses were assessed 7 days post-exposure for retrospective classification into behavioral response groups. Brains were harvested for measurements of the glucocorticoid receptor, mineralocorticoid receptor, FK506-binding protein-51 and arginine vasopressin in specific brain regions to assess changes in hypothalamus–pituitary–adrenal axis (HPA) regulating factors. Methylprednisolone produced greater suppression of corticosterone in the PTSD-phenotype group. During the suppression, the PTSD-phenotype rats showed a significantly more pronounced pulsatile activity. In addition, the PTSD-phenotype group showed distinct changes in the ventral and dorsal CA1, dentate gyrus as well as in the paraventricular nucleus and supra-optic nucleus. These results demonstrate a pre-trauma vulnerability state that is characterized by an over-reactivity of the HPA and changes in its regulating factors.
AbstractList Previously, we found that basal corticosterone pulsatility significantly impacts the vulnerability for developing post-traumatic stress disorder (PTSD). Rats that exhibited PTSD-phenotype were characterized by blunted basal corticosterone pulsatility amplitude and a blunted corticosterone response to a stressor. This study sought to identify the mechanisms underlining both the loss of pulsatility and differences in downstream responses. Serial blood samples were collected manually via jugular vein cannula at 10-min intervals to evaluate suppression of corticosterone following methylprednisolone administration. The rats were exposed to predator scent stress (PSS) after 24 h, and behavioral responses were assessed 7 days post-exposure for retrospective classification into behavioral response groups. Brains were harvested for measurements of the glucocorticoid receptor, mineralocorticoid receptor, FK506-binding protein-51 and arginine vasopressin in specific brain regions to assess changes in hypothalamus–pituitary–adrenal axis (HPA) regulating factors. Methylprednisolone produced greater suppression of corticosterone in the PTSD-phenotype group. During the suppression, the PTSD-phenotype rats showed a significantly more pronounced pulsatile activity. In addition, the PTSD-phenotype group showed distinct changes in the ventral and dorsal CA1, dentate gyrus as well as in the paraventricular nucleus and supra-optic nucleus. These results demonstrate a pre-trauma vulnerability state that is characterized by an over-reactivity of the HPA and changes in its regulating factors.
Author Cohen, Hagit
Todder, Doron
Danan, Dor
Zohar, Joseph
AuthorAffiliation 1 Anxiety and Stress Research Unit, Beer-Sheva Mental Health Center, Ministry of Health, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer-Sheva 84170, Israel; doriandanan@gmail.com (D.D.); doron.todder1@PBSH.HEALTH.GOV.IL (D.T.)
2 Post-Trauma Center, Sheba Medical Center, Tel Aviv 52621, Israel; joseph.zohar@sheba.health.gov.il
AuthorAffiliation_xml – name: 1 Anxiety and Stress Research Unit, Beer-Sheva Mental Health Center, Ministry of Health, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer-Sheva 84170, Israel; doriandanan@gmail.com (D.D.); doron.todder1@PBSH.HEALTH.GOV.IL (D.T.)
– name: 2 Post-Trauma Center, Sheba Medical Center, Tel Aviv 52621, Israel; joseph.zohar@sheba.health.gov.il
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  fullname: Danan, Dor
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Snippet Previously, we found that basal corticosterone pulsatility significantly impacts the vulnerability for developing post-traumatic stress disorder (PTSD). Rats...
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SubjectTerms animal model
corticosterone
glucocorticoid receptor
hypothalamus–pituitary–adrenal axis
posttraumatic stress disorder
pulsatility
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Title Is PTSD-Phenotype Associated with HPA-Axis Sensitivity? Feedback Inhibition and Other Modulating Factors of Glucocorticoid Signaling Dynamics
URI https://search.proquest.com/docview/2548396429
https://pubmed.ncbi.nlm.nih.gov/PMC8200046
https://doaj.org/article/2f1c68fc4f114f349f93a9361d11dbff
Volume 22
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