Stress, glucocorticoid hormones, and hippocampal neural progenitor cells: implications to mood disorders
Open accessAbstract
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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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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- Authors
- Kino, T.
- Affiliations
- Sidra Medical and Research Center (QA)
- Corresponding author
- Kino, Tomoshige
- ORCID
- Kino, Tomoshige
- Venue
- Frontiers in Physiology
- Publisher
- Frontiers Media SA
- Published
- 2015-08-19
- Volume
- 6
- Pages
- 230-230
- ISSN
- 1664-042X (ISSN-L)
- PMC
- PMC4541029
- 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
- gold
- doi.org
- 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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