Conversion of psychological stress into cellular stress response: Roles of the sigma‐1 receptor in the process
Open accessAbstract
Psychiatrists empirically recognize that excessive or chronic psychological stress can result in long‐lasting impairments of brain functions that partly involve neuronal cell damage. Recent studies begin to elucidate the molecular pathways activated/inhibited by psychological stress. Activation of the hypothalamic–pituitary–adrenal axis under psychological stress causes inflammatory oxidative stresses in the brain, in part due to elevation of cytokines. Psychological stress or neuropathological conditions (e.g., accumulation of β‐amyloids) trigger ‘cellular stress responses’, which promote upregulation of molecular chaperones to protect macromolecules from degradation. The unfolded protein response, the endoplasmic reticulum (ER)‐specific cellular stress response, has been recently implicated in the pathophysiology of neuropsychiatric disorders and the pharmacology of certain clinically used drugs. The sigma‐1 receptor is an ER protein whose ligands are shown to exert antidepressant‐like and neuroprotective actions. Recent studies found that the sigma‐1 receptor is a novel ligand‐operated ER chaperone that regulates bioenergetics, free radical generation, oxidative stress, unfolded protein response and cytokine signaling. The sigma‐1 receptor also regulates morphogenesis of neuronal cells, such as neurite outgrowth, synaptogenesis, and myelination, which can be perturbed by cellular stress. The sigma‐1 receptor may thus contribute to a cellular defense system that protects nervous systems against chronic psychological stress. Findings from sigma receptor research imply that not only cell surface monoamine effectors but also intracellular molecules, especially those at the ER, may provide novel therapeutic targets for future drug developments.
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Environmental and external stress can lead to psychological stress and subsequent cellular stress exacerbated by inflammation and oxidative damage.
“Environmental and external stress can lead to psychological stress and the subsequent cellular stress exacerbated by inflammation and oxidative damage [553–555].”
From Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease (2020) · cites this paper as [554]
Inside the cell, Sig-1R is located mainly at the ER-mitochondrion interface (MAM) and regulates cellular bioenergetics, particularly under stressful conditions.
“Inside the cell Sig-1R is located mainly at the ER–mitochondrion interface—referred to as the MAM—and regulates cellular bioenergetics, particularly under stressful conditions (Su et al., 2010; Mori et al., 2013; Hayashi, 2015).”
From The therapeutic potentials of Ayahuasca: possible effects against various diseases of civilization (2016) · cites this paper as Hayashi, 2015
The Sig-1R located at the MAM is an excellent candidate for interfering with the conversion of environmental stress in general and psychological stress in particular into cellular stress response by its regulatory effect on signaling between the ER and mitochondrion.
“The Sig-1R located at the MAM is an excellent candidate for interfering with the conversion of environmental stress in general and psychological stress in particular into cellular stress response by its regulatory effect on signaling between the ER and mitochondrion (Hayashi, 2015).”
From The therapeutic potentials of Ayahuasca: possible effects against various diseases of civilization (2016) · cites this paper as Hayashi, 2015
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- Authors
- Hayashi, T.
- Affiliations
- Nishikawa Hospital (JP)
- Corresponding author
- Hayashi, Teruo
- Venue
- Psychiatry and Clinical Neurosciences
- Publisher
- Wiley
- Published
- 2015-02-16
- Volume
- 69
- Issue
- 4
- Pages
- 179-191
- ISSN
- 1323-1316 (ISSN-L)
- 1440-1819
- OpenAlex
- W1831522096
- Cited by
- 87
- References
- 103
- Citations by year
- 2026: 4 · 2025: 4 · 2024: 8 · 2023: 7 · 2022: 8 · 2021: 12 · 2020: 9 · 2019: 11 · 2018: 10 · 2017: 7 · 2016: 7
- FWCI
- 0.44
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Psychiatry and Clinical Neurosciences (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Pharmacological Receptor Mechanisms and Effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Endoplasmic Reticulum Stress and Disease
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Heat shock proteins research
- Keywords
- sigma-1 receptor, psychological stress, cellular stress response, endoplasmic reticulum stress, unfolded protein response, oxidative stress, neuroinflammation, cytokine signaling, hypothalamic-pituitary-adrenal axis, molecular chaperones, neuroprotection, antidepressant-like effects, neurite outgrowth, synaptogenesis, myelination, neurodegeneration, therapeutic target
- MeSH terms
- Sigma-1 Receptor, Animals, Humans, Hypothalamo-Hypophyseal System, Molecular Sequence Data, Pituitary-Adrenal System, Stress, Psychological, Receptors, sigma, Oxidative Stress
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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