A History of Corticosterone Exposure Regulates Fear Extinction and Cortical NR2B, GluR2/3, and BDNF
Open accessAbstract
A history of exposure to stressors may be a predisposing factor for developing posttraumatic stress disorder (PTSD) after trauma. Extinction of conditioned fear appears to be impaired in PTSD, but the consequences of prior stress or excess glucocorticoid exposure for extinction learning are not known. We report that prior chronic exposure to the stress hormone, corticosterone (CORT), decreases endogenous CORT secretion upon context reexposure and impairs extinction after contextual fear conditioning in rats, while leaving fear memory acquisition and expression intact. Posttraining administration of the glucocorticoid receptor (GR) antagonist, RU38486, partially mimicked prior CORT exposure effects on freezing during fear extinction training. Extinction of conditioned fear is an active learning process thought to involve glutamatergic targets--including specific NMDA and AMPA receptor subunits--in the ventromedial prefrontal cortex (vmPFC), which includes the prelimbic, infralimbic, and medial orbitofrontal cortices. After CORT exposure, decreases in the NMDA receptor NR2B subunit and AMPA receptor subunits, GluR2/3, as well as brain-derived neurotrophic factor, were detected in cortical regions, but not dorsal hippocampus (CA1). Receptor subunit expression levels in the vmPFC correlated with freezing during training. In addition, prior CORT selectively decreased sucrose preference, consistent with established models of anhedonia and with blunted affect in PTSD. Together, these data suggest a cellular mechanism by which chronically elevated glucocorticoid exposure--as may be experienced during repeated exposure to stressors--interferes with the neural systems that modulate behavioral flexibility and may thereby contribute to psychopathological fear states.
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Chronic glucocorticoid exposure reduces brain-derived neurotrophic factor levels in the PFC, as does chronic stress, but it is not yet known whether this contributes to the observed dendritic changes.
“Chronic glucocorticoid exposure also reduces brain-derived neurotrophic factor levels in the PFC119, as does chronic stress120, but it is not yet known whether this contributes to the observed dendritic changes.”
From Stress signalling pathways that impair prefrontal cortex structure and function (2009) · cites this paper as [119]
The Results (Prior CORT Selectively Regulates Cortical Targets; page unavailable) report reduced BDNF mRNA in the orbitofrontal cortex after chronic corticosterone exposure, supporting a reduction in one PFC region. They found no change in ventromedial PFC samples and did not measure BDNF protein, so the broader claim about PFC BDNF levels exceeds what was measured. Citation 119 is attached to the glucocorticoid finding, not the separate chronic-stress claim. (LLM, conf=0.86)
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- Authors
- Gourley, S. L., Kedves, A. T., Olausson, P., & Taylor, J. R.
- Affiliations
- Yale University (US)
- Corresponding author
- Taylor, Jane R
- Venue
- Neuropsychopharmacology
- Published
- 2008-08-20
- Volume
- 34
- Issue
- 3
- Pages
- 707-716
- ISSN
- 0893-133X (ISSN-L)
- 1740-634X
- PMC
- PMC3679657
- OpenAlex
- W2041329554
- Cited by
- 218
- References
- 12
- Citations by year
- 2026: 3 · 2025: 5 · 2024: 8 · 2023: 9 · 2022: 4 · 2021: 7 · 2020: 16 · 2019: 7 · 2018: 12 · 2017: 18 · 2016: 15 · 2015: 16 · 2014: 19 · 2013: 14 · 2012: 24
- FWCI
- 6.56
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Neuropsychopharmacology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- State of Connecticut Department of Mental Health and Addiction Services
- National Institute of Mental Health (MH 66172, MH 25642, MH 79680, P01MH025642, F31MH079680, P50MH066172)
- Topics
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Social Sciences › Psychology › Clinical Psychology › Posttraumatic Stress Disorder Research
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Keywords
- corticosterone, glucocorticoid exposure, fear extinction, post-traumatic stress disorder, contextual fear conditioning, ventromedial prefrontal cortex, NMDA receptor NR2B, AMPA receptor subunits, GluR2/3, brain-derived neurotrophic factor, glucocorticoid receptor, mifepristone, anhedonia, sucrose preference, behavioral flexibility, stress history
- MeSH terms
- Animals, Conditioning, Classical, Corticosterone, Extinction, Psychological, Fear, Hippocampus, Memory, Short-Term, Receptors, Glucocorticoid, Sucrose, Mifepristone, Receptors, N-Methyl-D-Aspartate, Rats, Sprague-Dawley, Prefrontal Cortex, Receptors, AMPA, Brain-Derived Neurotrophic Factor, Rats
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