Cited by 111Neurogenesis and neuroplasticity mechanismsStress Responses and CortisolMemory and Neural Mechanisms

Stress, glucocorticoid hormones, and hippocampal neural progenitor cells: implications to mood disorders

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Kino, Tomoshige·2015·Frontiers in Physiology

Abstract

The hypothalamic-pituitary-adrenal (HPA) axis and its end-effectors glucocorticoid hormones play central roles in the adaptive response to numerous stressors that can be either internal or external. Thus, this system has a strong impact on the brain hippocampus and its major functions, such as cognition, memory as well as behavior, and mood. The hippocampal area of the adult brain contains neural stem cells or more committed neural progenitor cells, which retain throughout the human life the ability of self-renewal and to differentiate into multiple neural cell lineages, such as neurons, astrocytes, and oligodendrocytes. Importantly, these characteristic cells contribute significantly to the above-indicated functions of the hippocampus, while various stressors and glucocorticoids influence proliferation, differentiation, and fate of these cells. This review offers an overview of the current understanding on the interactions between the HPA axis/glucocorticoid stress-responsive system and hippocampal neural progenitor cells by focusing on the actions of glucocorticoids. Also addressed is a further discussion on the implications of such interactions to the pathophysiology of mood disorders.

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Crossref · 10.3389/fphys.2015.00230

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  • Abnormal GR activation contributes to neuronal apoptosis and degeneration by reducing expression of BDNF and inhibiting cellular proliferation.

    “Abnormal GR activation contributes to neuronal apoptosis and degeneration by reducing the expression of BDNF and inhibiting cellular proliferation”

    From Serum/glucocorticoid regulated kinase 1 (SGK1) in neurological disorders: pain or gain (2024) · cites this paper as Kino, 2015

    The HPA-axis section (page unavailable) says high glucocorticoid levels mediated by GR can cause apoptosis in hippocampal neurons. The Glucocorticoids section (page unavailable) reports reduced hippocampal progenitor-cell proliferation and says high glucocorticoid doses inhibit production of brain-derived neurotrophic factor. It does not establish that reduced BDNF and proliferation cause neuronal apoptosis or degeneration, and it notes increased proliferation in a separate cortical stem-cell experiment. (LLM, conf=0.86)

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Research works printed but not linked: 1

  1. Kino T. Chrousos G. P. (2004a). Glucocorticoid effect on gene expression, in Handbook on Stress and the Brain Part 1, eds Steckler T. Kalin N. H. Reul J. M. Reul H. M. (Amsterdam: Elsevier BV), 295– 312.

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Authors
Kino, T.
Affiliations
Sidra Medical and Research Center (QA)
Corresponding author
Kino, Tomoshige
Venue
Frontiers in Physiology
Published
2015-08-19
Volume
6
Pages
230-230
ISSN
1664-042X (ISSN-L)
OpenAlex
W1953188466
Cited by
111
References
66
Citations by year
2026: 4 · 2025: 12 · 2024: 12 · 2023: 6 · 2022: 17 · 2021: 10 · 2020: 7 · 2019: 10 · 2018: 10 · 2017: 10 · 2016: 11 · 2015: 2
FWCI
1.37
Type
journal article
Language
en
Open access
Licence
cc-by
Locations
  • Frontiers in Physiology (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
Sidra Medicine
Topics
  • Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
  • Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
Keywords
hypothalamic-pituitary-adrenal axis, glucocorticoids, stress, mood disorders, neural stem cells, neurogenesis, self-renewal, cell differentiation, hippocampus

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