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Cited by 437Stress Responses and CortisolAdrenal Hormones and DisordersEstrogen and related hormone effects

Role of glucocorticoid negative feedback in the regulation of HPA axis pulsatility

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Gjerstad, Julia K, Lightman, Stafford L, Spiga, Francesca·2018·Stress
DOI 10.1080/10253890.2018.1470238PMC PMC6220752
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Abstract

The hypothalamic-pituitary-adrenal (HPA) axis is the major neuroendocrine axis regulating homeostasis in mammals. Glucocorticoid hormones are rapidly synthesized and secreted from the adrenal gland in response to stress. In addition, under basal conditions glucocorticoids are released rhythmically with both a circadian and an ultradian (pulsatile) pattern. These rhythms are important not only for normal function of glucocorticoid target organs, but also for the HPA axis responses to stress. Several studies have shown that disruption of glucocorticoid rhythms is associated with disease both in humans and in rodents. In this review, we will discuss our knowledge of the negative feedback mechanisms that regulate basal ultradian synthesis and secretion of glucocorticoids, including the role of glucocorticoid and mineralocorticoid receptors and their chaperone protein FKBP51. Moreover, in light of recent findings, we will also discuss the importance of intra-adrenal glucocorticoid receptor signaling in regulating glucocorticoid synthesis.

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  • Intermediate-action inhibition (genomic) has its onset at approximately 30-minutes to an hour after steroid administration and HPA-axis inhibition can last for hours.

    “In contrast, intermediate-action inhibition (i.e.genomic) has its onset at approximately 30-minutes to an hour after steroid administration and HPA-axis inhibition can last for hours.”

    From The effects of exercise intensity on the cortisol response to a subsequent acute psychosocial stressor. (2021) · cites this paper as Gjerstad et al., 2018

    In “An overview of the hypothalamic–pituitary–adrenal axis and its rhythms” (page unavailable), the review describes genomic negative feedback as delayed and occurring over hours to days, supporting prolonged HPA-axis inhibition. It does not give an onset of 30 minutes to an hour after steroid administration; that timing is not supported by our copy. (LLM, conf=0.85)

    Experimental — accuracy not yet measured

  • The intermediate-time effect weakens excitability in the HPA-axis more substantially than fast-action inhibition without fully abolishing it.

    “This intermediate-time effect weakens excitability in the HPA-axis more substantially than fast-action inhibition without fully abolishing it.”

    From The effects of exercise intensity on the cortisol response to a subsequent acute psychosocial stressor. (2021) · cites this paper as Gjerstad et al., 2018

    The overview of the hypothalamic–pituitary–adrenal axis (page unavailable) distinguishes fast inhibition from delayed feedback, and the ACTH synthesis and secretion section describes reduced corticotroph bursting. Our copy does not say that an intermediate-time effect weakens HPA-axis excitability more than fast inhibition, or that it does so without fully abolishing excitability. (LLM, conf=0.78)

    Experimental — accuracy not yet measured

  • Intermediate-action inhibition seems to rely on genomic alterations at the level of protein synthesis and epigenetic modification of intra-cellular signaling mechanisms.

    “It seems to rely on genomic alterations at the level of protein synthesis and epigenetic modification of intra-cellular signaling mechanisms (Gjerstad et al., 2018;Keller-Wood and Dallman, 1984).”

    From The effects of exercise intensity on the cortisol response to a subsequent acute psychosocial stressor. (2021) · cites this paper as Gjerstad et al., 2018

    The sections on ACTH synthesis and corticosterone synthesis describe glucocorticoid negative feedback through changes in gene transcription, supporting the genomic part of the claim. Our copy does not identify these as intermediate-action inhibition or say that this inhibition relies on epigenetic modification of intracellular signaling mechanisms; its explicit mention of epigenetics is in a reference title, not that account. (LLM, conf=0.83)

    Experimental — accuracy not yet measured

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Authors
Gjerstad, J. K., Lightman, S. L., & Spiga, F.
Affiliations
University of Bristol (GB)
Corresponding author
Spiga, Francesca
ORCID
Venue
Stress
Publisher
Informa UK Limited
Published
2018-05-15
Volume
21
Issue
5
Pages
403-416
ISSN
  • 1025-3890 (ISSN-L)
  • 1607-8888
DOI
10.1080/10253890.2018.1470238
PMC
PMC6220752
OpenAlex
W2804081205
Cited by
437
References
191
Citations by year
2026: 51 · 2025: 44 · 2024: 87 · 2023: 62 · 2022: 65 · 2021: 69 · 2020: 43 · 2019: 13 · 2018: 3
FWCI
3.60
Type
journal article
Language
en
Open access
Licence
Locations
  • Stress (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • Bristol Research (University of Bristol) (submittedVersion, other-oa)
Funders
  • Medical Research Council (MR/J008893/1)
  • Neuroendocrinology Charitable Trust
Topics
  • Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adrenal Hormones and Disorders
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
Keywords
glucocorticoid negative feedback, ultradian rhythms, circadian rhythm, glucocorticoid receptor, mineralocorticoid receptor, FKBP51, stress response
MeSH terms
Adrenal Glands, Animals, Circadian Rhythm, Glucocorticoids, Homeostasis, Humans, Hypothalamo-Hypophyseal System, Pituitary-Adrenal System, Receptors, Glucocorticoid, Signal Transduction, Feedback, Physiological

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