BDNF and glucocorticoids regulate corticotrophin-releasing hormone (CRH) homeostasis in the hypothalamus
Open accessAbstract
Regulation of the hypothalamic–pituitary–adrenal (HPA) axis is critical for adaptation to environmental changes. The principle regulator of the HPA axis is corticotrophin-releasing hormone (CRH), which is made in the parventricular nucleus and is an important target of negative feedback by glucocorticoids. However, the molecular mechanisms that regulate CRH are not fully understood. Disruption of normal HPA axis activity is a major risk factor of neuropsychiatric disorders in which decreased expression of the glucocorticoid receptor (GR) has been documented. To investigate the role of the GR in CRH neurons, we have targeted the deletion of the GR, specifically in the parventricular nucleus. Impairment of GR function in the parventricular nucleus resulted in an enhancement of CRH expression and an up-regulation of hypothalamic levels of BDNF and disinhibition of the HPA axis. BDNF is a stress and activity-dependent factor involved in many activities modulated by the HPA axis. Significantly, ectopic expression of BDNF in vivo increased CRH, whereas reduced expression of BDNF, or its receptor TrkB, decreased CRH expression and normal HPA functions. We find the differential regulation of CRH relies upon the cAMP response-element binding protein coactivator CRTC2, which serves as a switch for BDNF and glucocorticoids to direct the expression of CRH.
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Targeted deletion of GR in the PVN increases CRH expression and CORT and ACTH levels in male mice.
“Additional evidence for CORT acting directly on PVN neurons comes from studies where targeted deletion of GR in the PVN increased CRH expression and CORT and ACTH levels in male mice (Jeanneteau et al., 2012).”
From Hypothalamic–pituitary–adrenal and hypothalamic–pituitary–gonadal axes: sex differences in regulation of stress responsivity (2017) · cites this paper as Jeanneteau et al., 2012
In “Reduced Expression of the GR in the PVN Disinhibits the HPA Axis,” the paper reports increased PVN CRH and elevated plasma ACTH and corticosterone in GR flox/+;Sim1Cre mice. The Methods specify adult males. The deletion was of one floxed GR allele, producing reduced GR expression rather than complete deletion; Sim1-Cre expression was also not confined to the PVN. (LLM, conf=0.87)
Experimental — accuracy not yet measuredCross-talk between BDNF and CRH may be at least partly mediated by the CREB and MAPK pathway and is involved in the enhancement of fear memory under stress.
“This cross-talk between BDNF and CRH may be at least partly mediated by the CREB and MAPK pathway and is involved in the enhancement of fear memory under stress (187).”
From Epigenetic Modifications in Stress Response Genes Associated With Childhood Trauma (2019) · cites this paper as [187]
The introductory section reports that BDNF signaling affects hypothalamic CRH through CREB and its coactivator CRTC2; the CRTC2 section also links CREB to BDNF-dependent CRH regulation (page numbers unavailable). The cited paper does not establish MAPK mediation or involvement in enhanced fear memory under stress. (LLM, conf=0.87)
Experimental — accuracy not yet measuredAdministration of BDNF in vivo induces increased CRH level and reduction of BDNF or its receptor normalizes the CRH level and thus the HPA axis.
“The administration of BDNF in vivo induces increased CRH level and reduction of BDNF or its receptor normalizes the CRH level and thus, the HPA axis.”
From Epigenetic Modifications in Stress Response Genes Associated With Childhood Trauma (2019) · cites this paper as [187]
The Ectopic Expression section reports that increasing BDNF in mice increased CRH protein. The Maintenance of HPA Axis Reactivity section and Discussion report that reduced TrkB or BDNF lowered CRH and HPA-axis measures, not that it normalized CRH or the HPA axis. (LLM, conf=0.90)
Experimental — accuracy not yet measuredThere is a feedback loop whereby BDNF directly regulates CRH, and thus the HPA axis.
“Moreover, there is a feedback loop whereby directly regulates CRH, and thus, the HPA axis (187).”
From Epigenetic Modifications in Stress Response Genes Associated With Childhood Trauma (2019) · cites this paper as [187]
BDNF expression level responds to stress-related HPA axis activation.
“For BDNF, its expression level responds to stress-related HPA axis activation.”
From Epigenetic Modifications in Stress Response Genes Associated With Childhood Trauma (2019) · cites this paper as [187]
BDNF directly regulates the HPA axis.
“BDNF directly regulates the HPA axis.”
From Epigenetic Modifications in Stress Response Genes Associated With Childhood Trauma (2019) · cites this paper as [187]
Broad disruption of the GR allele in the CNS and its targeted deletion in the forebrain or PVN resulted in disinhibition of the HPA axis.
“Finally, the broad disruption of the GR allele in the CNS [GRNesCre (5)] and its targeted deletion in the forebrain [forebrain-specific GR knock-out; FBGRKO mice] (119), or the PVN all resulted in the disinhibition of the HPA axis (120).”
From The HPA – Immune Axis and the Immunomodulatory Actions of Glucocorticoids in the Brain (2014) · cites this paper as [120]
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- Authors
- Jeanneteau, F. D., Lambert, W. M., Ismaili, N., Bath, K. G., Lee, F. S., Garabedian, M. J., & Chao, M. V.
- Affiliations
- New York University (US)
- Department of Microbiology, New York University School of Medicine, New York, NY 10016;
- Brown University (US)
- Weill Cornell Medicine (US)
- Department of Cell Biology, Department of Physiology, Department of Neuroscience, and Department of Psychiatry, Skirball Institute of Biomolecular Medicine, and
- ORCID
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2012-01-09
- Volume
- 109
- Issue
- 4
- Pages
- 1305-1310
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC3268297
- OpenAlex
- W2021067562
- Cited by
- 252
- References
- 38
- Citations by year
- 2026: 11 · 2025: 11 · 2024: 18 · 2023: 12 · 2022: 12 · 2021: 17 · 2020: 18 · 2019: 18 · 2018: 18 · 2017: 27 · 2016: 19 · 2015: 17 · 2014: 15 · 2013: 24 · 2012: 15
- FWCI
- 9.42
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Alliance for Research on Schizophrenia and Depression
- National Institute of Biomedical Innovation
- National Institutes of Health (NS-21072)
- National Institute of Mental Health (R01MH086651, MH086651)
- National Institute of Allergy and Infectious Diseases (5T32 AI07180-29, T32AI007180)
- National Institute of Neurological Disorders and Stroke (R01NS021072, NS-21072, R56NS021072)
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Keywords
- brain-derived neurotrophic factor, glucocorticoids, corticotropin-releasing factor, hypothalamic-pituitary-adrenal axis, hypothalamus, glucocorticoid receptor, CRTC2, TrkB receptor, CREB, stress response, negative feedback
- MeSH terms
- Analysis of Variance, Animals, Corticotropin-Releasing Hormone, Glucocorticoids, Homeostasis, Hypothalamo-Hypophyseal System, Hypothalamus, Immunohistochemistry, Mice, Inbred C57BL, Neurons, Pituitary-Adrenal System, Receptors, Glucocorticoid, Transcription Factors, Trans-Activators, Mutagenesis, Site-Directed, Rats, Sprague-Dawley, Mice, Knockout, Microscopy, Confocal, Brain-Derived Neurotrophic Factor, Chromatin Immunoprecipitation, Mice, Rats, Real-Time Polymerase Chain Reaction
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