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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Factors promoting vulnerability to dysregulated stress reactivity and stress-related disease

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Russell, Ashley L. [1, 2] ; Tasker, Jeffrey G. [3] ; Lucion, Aldo B. [4] ; Fiedler, Jenny [5] ; Munhoz, Carolina D. [6] ; Wu, Tao-yiao John [1, 2, 7] ; Deak, Terrence [8]
Total Authors: 7
[1] Uniformed Serv Univ Hlth Sci, Program Neurosci, Bethesda, MD 20814 - USA
[2] Ctr Neurosci & Regenerat Med, Bethesda, MD - USA
[3] Tulane Univ, Dept Cell & Mol Biol, New Orleans, LA 70118 - USA
[4] Fed Univ Rio Grande Sul UFRGS, Inst Basic Hlth Sci ICBS, Dept Physiol, Porto Alegre, RS - Brazil
[5] Univ Chile, Chem & Pharmaceut Sci Fac, Dept Biochem & Mol Biol, Santiago - Chile
[6] Univ Sao Paulo, Inst Biomed Sci, Deparment Pharmacol, Sao Paulo - Brazil
[7] Uniformed Serv Univ Hlth Sci, Dept Obstet & Gynecol, Bethesda, MD 20814 - USA
[8] Binghamton Univ, Behav Neurosci Program, Dept Psychol, DEARC, Binghamton, NY - USA
Total Affiliations: 8
Document type: Review article
Source: Journal of Neuroendocrinology; v. 30, n. 10, SI OCT 2018.
Web of Science Citations: 6

Effective coordination of the biological stress response is integral for the behavioural well-being of an organism. Stress reactivity is coordinated by an interplay of the neuroendocrine system and the sympathetic nervous system. The hypothalamic-pituitary-adrenal (HPA) axis plays a key role in orchestrating the bodily responses to stress, and the activity of the axis can be modified by a wide range of experiential events. This review focuses on several factors that influence subsequent HPA axis reactivity. Some of these factors include early-life adversity, exposure to chronic stress, immune activation and traumatic brain injury. The central premise is that each of these experiences serves as a general vulnerability factor that accelerates future HPA axis reactivity in ways that make individuals more sensitive to stress challenges, therefore feeding forward into the exacerbation of ongoing (or greater susceptibility toward) future stress-related disease states, especially as they pertain to negative affect and overall brain health. (AU)

FAPESP's process: 12/24727-4 - Comparison of the therapeutical effects of dexamethasone (a synthetic glucocorticoid analogue), and G1 (a G-coupled estrogen receptor, GPER agonist) on the EAE-induced neuroinflammation
Grantee:Carolina Demarchi Munhoz
Support type: Regular Research Grants
FAPESP's process: 16/03572-3 - The relationship between glucocorticoid receptor activation and the neuronal hyperexcitability in the basolateral amygdala in the restraint stress-induced long-lasting anxiety and their implications in the impaired contextual fear extinction
Grantee:Carolina Demarchi Munhoz
Support type: Regular Research Grants