Rapid non-genomic effects of corticosteroids and their role in the central stress response
Open accessAbstract
In response to a stressful encounter, the brain activates a comprehensive stress system that engages the organism in an adaptive response to the threatening situation. This stress system acts on multiple peripheral tissues and feeds back to the brain; one of its key players is the family of corticosteroid hormones. Corticosteroids affect brain functioning through both delayed, genomic and rapid, non-genomic mechanisms. The latter mode of action has long been known, but it is only in recent years that the physiological basis in the brain is beginning to be unravelled. We now know that corticosteroids exert rapid, non-genomic effects on the excitability and activation of neurons in (amongst others) the hypothalamus, hippocampus, amygdala and prefrontal cortex. In addition, corticosteroids affect cognition, adaptive behaviour and neuroendocrine output within minutes. Knowledge on the identity of the receptors and secondary pathways mediating the non-genomic effects of corticosteroids on a cellular level is accumulating. Interestingly, in many cases, an essential role for the ‘classical’ mineralocorticoid and glucocorticoid receptors in a novel membrane-associated mechanism is found. Here, we systematically review the recent literature on non-genomic actions of corticosteroids on neuronal activity and functioning in selected limbic brain targets. Further, we discuss the relevance of these permissive effects for cognition and neuroendocrine control, and the integration of this novel mode of action into the complex balanced pattern of stress effects in the brain.
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Activation of the HPA axis is known to induce glutamatergic strengthening.
“Consistent with the correlation between FM and acute or chronic stress, the activation of the HPA axis is known to induce glutamatergic strengthening [59–61].”
From Fibromyalgia pathogenesis explained by a neuroendocrine multistable model (2024) · cites this paper as [59]
The Prefrontal cortex section reports that acute stress or corticosterone increased glutamatergic transmission, supporting the claim in that setting. But it also reports reduced plasticity under chronic stress, and the Regulation of the HPA-axis section describes corticosterone suppressing glutamatergic transmission in the hypothalamus. The unqualified claim that HPA-axis activation induces glutamatergic strengthening is therefore broader than the paper supports; page numbers were not available in our copy. (LLM, conf=0.86)
Experimental — accuracy not yet measuredUpregulation of β-adrenergic GPCR signaling by catecholaminergic and nongenomic actions of glucocorticoid receptor signaling activates cAMP and calcium signaling that influence TCA enzymes and oxidative phosphorylation for production of NADH and ATP.
“The upregulation of β-adrenergic GPCR signaling by catecholaminergic and nongenomic actions of glucocorticoid receptor signaling (29) is known to activate cAMP and calcium signaling that influence TCA enzymes and oxidative phosphorylation for production of NADH and ATP, respectively.”
From Mechanistic inferences on metabolic dysfunction in posttraumatic stress disorder from an integrated model and multiomic analysis: role of glucocorticoid receptor sensitivity (2019) · cites this paper as [29]
Split into 2 atoms — 0 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 1 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredGlutamatergic transmission is positively correlated with stress-induced glucocorticoids, notably cortisol.
“whereas glutamatergic transmission is positively correlated with stress-induced glucocorticoids, notably cortisol.”
From Fibromyalgia pathogenesis explained by a neuroendocrine multistable model (2024) · cites this paper as [59]
The Concluding remarks (Figure 2; page unavailable) describe corticosterone facilitating glutamatergic transmission, which supports a positive effect in some pathways. But the same passage describes inhibition in the hypothalamus and amygdala. It does not establish a general positive correlation or identify cortisol specifically as producing that pattern. (LLM, conf=0.87)
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“GR, a prototype member of nuclear receptor superfamily (designated as NR3C1 in nomenclature of nuclear receptor family) is a ligand-activated transcription factor, it can also exert non-genomic actions (Groeneweg et al., 2011).”
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- Authors
- Groeneweg, F. L., Karst, H., de Kloet, E. R., & Joëls, M.
- Affiliations
- Leiden University (NL)
- University Medical Center Utrecht (NL)
- Corresponding author
- Groeneweg, Femke L
- Venue
- Journal of Endocrinology
- Publisher
- Bioscientifica
- Published
- 2011-02-28
- Volume
- 209
- Issue
- 2
- Pages
- 153-167
- ISSN
- 0022-0795 (ISSN-L)
- 1479-6805
- OpenAlex
- W2149369024
- Semantic Scholar
- 35e8a99cce2b4537123c404c8674c828b3da82c2
- Cited by
- 414
- References
- 138
- Citations by year
- 2026: 11 · 2025: 13 · 2024: 16 · 2023: 19 · 2022: 13 · 2021: 24 · 2020: 27 · 2019: 35 · 2018: 30 · 2017: 30 · 2016: 31 · 2015: 31 · 2014: 45 · 2013: 34 · 2012: 42
- FWCI
- 3.60
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Endocrinology (publishedVersion)
- PubMed (publishedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- Leiden Repository (Leiden University) (submittedVersion)
- Funders
- Koninklijke Nederlandse Akademie van Wetenschappen
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- corticosteroids, hypothalamus, hippocampus, amygdala, prefrontal cortex, neuronal excitability, mineralocorticoid receptor, glucocorticoid receptor, cell surface receptors, cognition, neuroendocrine regulation, limbic system
- MeSH terms
- Animals, Behavior, Animal, Brain, Cognition, Corticosterone, Humans, Neurosecretory Systems, Stress, Physiological
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