Role of the Hippocampus, the Bed Nucleus of the Stria Terminalis, and the Amygdala in the Excitatory Effect of Corticotropin-Releasing Hormone on the Acoustic Startle Reflex
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Previously, we demonstrated that transection of the fimbria/fornix blocked the excitatory effect of corticotropin-releasing hormone (CRH) on startle (CRH-enhanced startle), suggesting that the hippocampus and its efferent target areas that communicate via the fimbria may be critically involved in CRH-enhanced startle. The bed nucleus of the stria terminalis (BNST) receives direct projections from the ventral hippocampus via the fimbria/fornix. Therefore, the role of the ventral hippocampus, the BNST, and the amygdala in CRH-enhanced startle was investigated. NMDA lesions of the BNST completely blocked CRH-enhanced startle, whereas chemical lesions of the ventral hippocampus and the amygdala failed to block CRH-enhanced startle. However, the same amygdala-lesioned animals showed a complete blockade of fear-potentiated startle, a conditioned fear response sensitive to manipulations of the amygdala. In contrast, BNST-lesioned rats had normal fear-potentiated startle. This indicates a double dissociation between the BNST and the amygdala in two different paradigms that enhance startle amplitude. Microinfusions of CRH into the BNST, but not into the ventral hippocampus, mimicked intracerebroventricular CRH effects. Furthermore, infusion of a CRH antagonist into the BNST blocked CRH-enhanced startle in a dose-dependent manner. Control studies showed that this blockade did not result from either leakage of the antagonist into the ventricular system or a local anesthetic effect caused by infusion of the antagonist into the BNST. The present studies strongly suggest that CRH in the CSF can activate the BNST, which could lead to activation of brainstem and hypothalamic BNST target areas involved in anxiety and stress responses.
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CRF-enhanced startle depends on BNSTL, not CeA: BNSTL lesions or local CRF antagonist blocked it, while CeA manipulations did not.
“We also found that the BNSTL, but not the CeA, was involved in CRF-enhanced startle. For instance, excitotoxic BNSTL lesions, or local infusions of a CRF antagonist into the BNSTL, completely blocked CRF-enhanced startle, although similar lesions of the CeA, or infusions into the CeA, did not”
From Phasic vs Sustained Fear in Rats and Humans: Role of the Extended Amygdala in Fear vs Anxiety (2010) · cites this paper as Lee and Davis, 1997
The chemical-lesion Results report that BNST lesions completely blocked CRH-enhanced startle, whereas CeA lesions did not. The intra-BNST infusion Results report a dose-dependent attenuation by the CRH antagonist—not complete blockade—and the intra-CeA infusion Results report no blockade. The paper identifies the targeted region as BNST, without establishing the more specific BNSTL designation in these passages (page numbers unavailable). (LLM, conf=0.87)
Experimental — accuracy not yet measuredBNST infusion of the CRF1 antagonist blocked sustained fear to the 8-min clicker, whereas CeA infusion of a CRF antagonist did not affect phasic fear.
“We also found that local infusion into the BNST of this CRF1 antagonist blocked sustained fear to the 8-min clicker, in contrast to the lack of effect of the local infusion of a CRF antagonist into the CeA on phasic fear”
From Phasic vs Sustained Fear in Rats and Humans: Role of the Extended Amygdala in Fear vs Anxiety (2010) · cites this paper as Lee and Davis, 1997
The section on intra-CeA infusion reports that the CRH antagonist did not block light-cued fear-potentiated startle, supporting the phasic-fear comparison. The intra-BNST results instead report attenuation of startle enhanced by infused CRH; they do not report sustained fear to an 8-minute clicker. Page numbers are unavailable in our copy. (LLM, conf=0.90)
Experimental — accuracy not yet measuredA CRF antagonist infused into the central amygdala failed to block CRF-enhanced startle.
“a CRF antagonist infused into the CeA failed to block CRF-enhanced startle (Lee and Davis, 1997)”
From Phasic vs Sustained Fear in Rats and Humans: Role of the Extended Amygdala in Fear vs Anxiety (2010) · cites this paper as Lee and Davis, 1997
In the same lesioned rats tested for CRF-enhanced startle, central amygdala lesions, but not bed nucleus of the stria terminalis lesions, disrupted fear-potentiated startle.
“Lee and Davis (1997) confirmed that CeA, but not BNST, lesions disrupted fear-potentiated startle.”
From Phasic vs Sustained Fear in Rats and Humans: Role of the Extended Amygdala in Fear vs Anxiety (2010) · cites this paper as Lee and Davis (1997)
Excitotoxic lesions of the bed nucleus of the stria terminalis, but not the central amygdala, blocked CRF-enhanced startle.
“excitotoxic lesions of the BNST, but not the CeA, blocked CRF-enhanced startle”
From Phasic vs Sustained Fear in Rats and Humans: Role of the Extended Amygdala in Fear vs Anxiety (2010) · cites this paper as Lee and Davis (1997)
Intra-bed nucleus of the stria terminalis CRF infusions mimicked the effect of intraventricular infusions.
“intra-BNST CRF infusions mimicked the effect of intra-ventricular infusions.”
From Phasic vs Sustained Fear in Rats and Humans: Role of the Extended Amygdala in Fear vs Anxiety (2010) · cites this paper as Lee and Davis (1997)
The bed nucleus of the stria terminalis is the likely location of the CRF receptors that mediate the increase in startle after intracerebroventricular CRF infusion.
“Lee and Davis (1997) identified the BNST as the likely location of the CRF receptors that mediated the increase in startle after CRF is infused i.c.v.”
From Phasic vs Sustained Fear in Rats and Humans: Role of the Extended Amygdala in Fear vs Anxiety (2010) · cites this paper as Lee and Davis (1997)
Infusion of the CRF receptor antagonist α-helical CRF9-41 into the bed nucleus of the stria terminalis, but not into the central amygdala, blocked CRF-enhanced startle.
“infusion of the CRF receptor antagonist α-helical CRF9–41 (αhCRF) into the BNST, but not into the CeA, also blocked CRF-enhanced startle”
From Phasic vs Sustained Fear in Rats and Humans: Role of the Extended Amygdala in Fear vs Anxiety (2010) · cites this paper as Lee and Davis (1997)
BNST lesions abolish anxiety-like responses to bright light and CRH but do not affect conditioned fear, demonstrating a double dissociation between the amygdala and BNST.
“in contrast to amygdala lesions, BNST lesions abolished anxiety-like response to both bright light and CRH infusion (Lee and Davis, 1997;Walker and Davis, 1997); importantly, BNST lesions did not affect conditioned fear, demonstrating a double dissociation between the amygdala and BNST.”
From The human BNST: functional role in anxiety and addiction (2016) · cites this paper as Lee and Davis, 1997
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“For instance, excitotoxic BNSTL lesions, or local infusions of a CRF antagonist into the BNSTL, completely blocked CRF-enhanced startle, although similar lesions of the CeA, or infusions into the CeA, did not (Lee and Davis, 1997).”
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- Authors
- Lee, Y., & Davis, M.
- Affiliations
- Yale University (US)
- ORCID
- Davis, Michael
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 1997-08-15
- Volume
- 17
- Issue
- 16
- Pages
- 6434-6446
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC6568348
- OpenAlex
- W1754932253
- Cited by
- 457
- References
- 67
- Citations by year
- 2026: 4 · 2025: 10 · 2024: 11 · 2023: 9 · 2022: 13 · 2021: 6 · 2020: 11 · 2019: 14 · 2018: 13 · 2017: 15 · 2016: 16 · 2015: 16 · 2014: 17 · 2013: 22 · 2012: 10
- FWCI
- 11.34
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Neuroscience (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Mental Health (MH 47840, MH 00004)
- Air Force Office of Scientific Research
- Topics
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- corticotropin-releasing factor, acoustic startle response, bed nucleus of the stria terminalis, ventral hippocampus, amygdala, fear-potentiated startle, NMDA lesions, fimbria-fornix, hypothalamic-pituitary-adrenal axis, stress response, anxiety
- MeSH terms
- Acoustic Stimulation, Amygdala, Animals, Anxiety, Corticotropin-Releasing Hormone, Fear, Hippocampus, Hormone Antagonists, Injections, Intraventricular, Male, Peptide Fragments, Septal Nuclei, Reflex, Startle, Rats, Sprague-Dawley, Rats
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