The DOI matches its Crossref record; 152 of the 152 references it cites were found in a registry or an index.
Neural Regulation of the Stress Response: The Many Faces of Feedback
Open accessAbstract
The mammalian stress response is an integrated physiological and psychological reaction to real or perceived adversity. Glucocorticoids (GCs) are an important component of this response, acting to redistribute energy resources to both optimize survival in the face of challenge and restore homeostasis after the immediate threat has subsided. Release of GCs is mediated by the hypothalamo–pituitary–adrenocortical (HPA) axis, driven by a neural signal originating in the paraventricular nucleus (PVN). Stress levels of GCs bind to glucocorticoid receptors (GRs) in multiple body compartments, including brain, and consequently have wide-reaching actions. For this reason, GCs serve a vital function in feedback inhibition of their own secretion. Fast, non-genomic feedback inhibition of the HPA axis is mediated at least in part by GC signaling in the PVN, acting by a cannabinoid-dependent mechanism to rapidly reduce both neural activity and GC release. Delayed feedback termination of the HPA axis response is mediated by forebrain GRs, presumably by genomic mechanisms. GCs also act in the brainstem to attenuate neuropeptidergic excitatory input to the PVN via acceleration of mRNA degradation, providing a mechanism to attenuate future responses to stressors. Thus, rather than having a single defined feedback switch, GCs work through multiple neurocircuits and signaling mechanisms to coordinate HPA axis activity to suit the overall needs of multiple body systems.
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“Dysfunctional GCC signaling is implicated in chronic pain disorders, such as fibromyalgia and neuropathic pain, where alterations in GCC expression or sensitivity may influence the body’s ability to control inflammation and modulate the nociceptive response [135].”
From The Role of Cortisol in Chronic Stress, Neurodegenerative Diseases, and Psychological Disorders (2023) · cites this paper as [135]
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“The GCC is essential for modulating the anti-inflammatory and immunosuppressive actions of cortisol [135].”
From The Role of Cortisol in Chronic Stress, Neurodegenerative Diseases, and Psychological Disorders (2023) · cites this paper as [135]
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Citations
Cites
Stress and the brain: from adaptation to disease
de Kloet, E. R., Joëls, M., & Holsboer, F. (2005) · Nature Reviews Neuroscience · doi:10.1038/nrn1683 · Cited by 4,621 · cited 2×
“Although the permissive actions of MR maintain cellular responses to GCs, only stress levels of GCs extensively bind GR, which is necessary for the inhibition of HPA stress responses (Reul and de Kloet 1985; de Kloet and Reul 1987; Boyle et al. 2005; de Kloet et al. 2005).”
Deep Brain Stimulation for Treatment-Resistant Depression
Mayberg, H. S., Lozano, A. M., Voon, V., McNeely, H. E., Seminowicz, D., Hamani, C., Schwalb, J. M., & Kennedy, S. H. (2005) · Neuron · doi:10.1016/j.neuron.2005.02.014 · Cited by 4,059 · cited 2×
“…correlate with altered activation or volume of the prefrontal cortex, amygdala, and hippocampus, suggesting that the disease processes involve the anticipatory stress response (Drevets 1999; Mayberg et al. 2005; Yehuda and LeDoux 2007; Krishnan and Nestler 2010; Myers-Schulz and Koenigs 2011).”
Vale, W., Spiess, J., Rivier, C., & Rivier, J. (1981) · Science · doi:10.1126/science.6267699 · Cited by 3,965
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“These neurons project to blood vessels in the median eminence, where they release adrenocorticotropin (ACTH) secretagogues, the most potent of which are corticotropin-releasing hormone (CRH) and arginine vasopressin (Vale et al. 1981; Swanson et al. 1983).”
Neural regulation of endocrine and autonomic stress responses
Ulrich-Lai, Y. M., & Herman, J. P. (2009) · Nature Reviews Neuroscience · doi:10.1038/nrn2647 · Cited by 3,318 · cited 6×
“, the nucleus of the solitary tract (NTS), circumventricular organs) (Ulrich-Lai and Herman 2009).”
InfluentialSelf-citationBrain corticosteroid receptor balance in health and disease
de Kloet, E. R., Vreugdenhil, E., Oitzl, M. S., & Joëls, M. (1998) · Endocrine Reviews · doi:10.1210/edrv.19.3.0331 · Cited by 2,614 · cited 1×
“The MR has a very high affinity for endogenous GCs and regulates circadian secretory rhythms and ultradian pulsatility (de Kloet et al. 1998; de Kloet and Sarabdjitsingh 2008).”
Brain corticosteroid receptor balance in health and disease
de Kloet, E. R. (1998) · Endocrine Reviews · doi:10.1210/er.19.3.269 · Cited by 2,614
Two receptor systems for corticosterone in rat brain: Microdistribution and differential occupation
REUL, J. M. H. M., & KLOET, E. R. D. (1985) · Endocrinology · doi:10.1210/endo-117-6-2505 · Cited by 2,580 · cited 1×
“Keywords Hypothalamo–pituitary–adrenocortical axis Corticotropin-releasing hormone Corticosterone Glucocorticoid receptor Hypothalamus Amygdala Prefrontal cortex”
The Neuroendocrinology of Stress and Aging: The Glucocorticoid Cascade Hypothesis
Sapolsky, R. M., Krey, L. C., & McEwen, B. S. (1986) · Science of Aging Knowledge Environment · doi:10.1126/sageke.2002.38.cp21 · Cited by 2,343
Swanson, L. W., Sawchenko, P. E., Rivier, J., & Vale, W. W. (2008) · Neuroendocrinology · doi:10.1159/000123454 · Cited by 1,953 · cited 1×
“These neurons project to blood vessels in the median eminence, where they release adrenocorticotropin (ACTH) secretagogues, the most potent of which are corticotropin-releasing hormone (CRH) and arginine vasopressin (Vale et al. 1981; Swanson et al. 1983).”
Cited by
Sorted by citations
Regulation of the Hypothalamic‐Pituitary‐Adrenocortical Stress Response
Herman, J. P., McKlveen, J. M., Ghosal, S., Kopp, B., Wulsin, A., Makinson, R., Scheimann, J., & Myers, B. (2016) · Comprehensive Physiology · doi:10.1002/cphy.c150015 · Cited by 1,819
“Control of glucocorticoid release is mediated by glucocorticoid feedback at varying levels of the HPA axis, serving to limit prolonged exposure to catabolic actions of glucocorticoids (117).”
Self-citationThe chronic mild stress (CMS) model of depression: History, evaluation and usage
Willner, P. (2017) · Neurobiology of Stress · doi:10.1016/j.ynstr.2016.08.002 · Cited by 959
“…been reported for an inhibitor of the glycine transporter GlyT1 (Depoort ere et al., 2005), and following epigenetic induction of mGlu2 receptors (Nasca et al., 2013), two treatments that might be expected to potentiate glutamatergic transmission at NMDA receptors (Cubelos et al., 2005;…”
BackgroundThe Role of Cortisol in Chronic Stress, Neurodegenerative Diseases, and Psychological Disorders
Knezevic, E., Nenic, K., Milanovic, V., & Knezevic, N. N. (2023) · Cells · doi:10.3390/cells12232726 · Cited by 564
“[135].”
BackgroundInfluentialBrowning, K. N., & Travagli, R. A. (2014) · Comprehensive Physiology · doi:10.1002/cphy.c130055 · Cited by 541
“…addition to exerting multiple effects throughout the periphery, corticosteroids also exert profound effects on several CNS nuclei [reviewed in (220,347)], including (i) activation of the CeA, BNST, PVN (regions which provide innervation to the LC) as well as the LC itself, (ii) the upregulation…”
Neural control of chronic stress adaptation
Herman, J. P. (2013) · Frontiers in Behavioral Neuroscience · doi:10.3389/fnbeh.2013.00061 · Cited by 384
Self-citation
Metadata
- Authors
- Myers, B., McKlveen, J. M., & Herman, J. P.
- Affiliations
- University of Cincinnati (US)
- Corresponding author
- Myers, Brent
- Venue
- Cellular and Molecular Neurobiology
- Published
- 2012-02-01
- Volume
- 32
- Issue
- 5
- Pages
- 683-694
- ISSN
- 0272-4340 (ISSN-L)
- 1573-6830
- PMC
- PMC3956711
- OpenAlex
- W2004982081
- Semantic Scholar
- ab6597d145f936c7638a64a02075f0bd9d576ebc
- Cited by
- 175
- References
- 151
- Citations by year
- 2026: 5 · 2025: 13 · 2024: 8 · 2023: 10 · 2022: 23 · 2021: 10 · 2020: 13 · 2019: 11 · 2018: 16 · 2017: 11 · 2016: 14 · 2015: 15 · 2014: 12 · 2013: 11 · 2012: 3
- FWCI
- 5.49
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Cellular and Molecular Neurobiology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute of Mental Health (R01MH049698, R21MH090574, R01MH069860, R01MH069725)
- National Institute of Diabetes and Digestive and Kidney Diseases (T32DK059803)
- National Institute of Neurological Disorders and Stroke (T32NS007453)
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adrenal Hormones and Disorders
- Keywords
- stress response, glucocorticoids, hypothalamic-pituitary-adrenal axis, paraventricular nucleus, glucocorticoid receptor, cannabinoid signaling, mRNA degradation, neuropeptide signaling, homeostasis, brainstem
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