Compensation in the neural circuitry of fear conditioning awakens learning circuits in the bed nuclei of the stria terminalis
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The basolateral amygdala (BLA) is thought to be essential for fear learning. However, extensive training can overcome the loss of conditional fear evident following lesions and inactivation of the BLA. Such results suggest the existence of a primary BLA-dependent and a compensatory BLA-independent neural circuit. We tested the hypothesis that the bed nuclei of the stria terminalis (BST) provides this compensatory plasticity. Using extensive context-fear conditioning, we demonstrate that combined BLA and BST lesions prevented fear acquisition and expression. Additionally, protein synthesis in the BST was critical only for consolidation of BLA-independent but not BLA-dependent fear. Moreover, fear acquired after BLA lesions resulted in greater activation of BST regions that receive hippocampal efferents. These results suggest that the BST is capable of functioning as a compensatory site in the acquisition and consolidation of context-fear memories. Unlocking such neural compensation holds promise for understanding situations when brain damage impairs normal function or failure to regulate compensatory sites leads to anxiety disorders.
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In the absence of a functional BLA, the BNST acts as a compensatory site in the acquisition of fear memories, although this BLA-independent fear learning requires more training.
“For example, in the absence of a functional BLA, the BNST acts as a compensatory site in the acquisition of fear memories, although this BLA-independent fear learning requires more training84.”
From Resolving the neural circuits of anxiety (2015) · cites this paper as [84]
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- Authors
- Poulos, A. M., Ponnusamy, R., Dong, H.-W., & Fanselow, M. S.
- Affiliations
- University of California, Los Angeles (US)
- Brain Research Institute, Niigata University (JP)
- Corresponding author
- Fanselow, Michael S.
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2010-08-02
- Volume
- 107
- Issue
- 33
- Pages
- 14881-14886
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC2930410
- OpenAlex
- W2121870210
- Cited by
- 104
- References
- 57
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 27 · 2023: 6 · 2022: 3 · 2021: 5 · 2020: 5 · 2019: 6 · 2018: 9 · 2017: 5 · 2016: 7 · 2015: 7 · 2014: 6 · 2013: 7 · 2012: 5
- FWCI
- 3.09
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Mental Health (R01MH062122, MH62122)
- Topics
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory Processes and Influences
- Keywords
- fear conditioning, basolateral amygdala, compensatory plasticity, fear consolidation, protein synthesis, neural compensation, anxiety disorders
- MeSH terms
- Amygdala, Animals, Conditioning, Psychological, Fear, Immunohistochemistry, Learning, Male, Memory, Nerve Net, Nerve Tissue Proteins, Neural Pathways, Neurons, Proto-Oncogene Proteins c-fos, Rats, Long-Evans, Antigens, Nuclear, Rats
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