Stress Leads to Contrasting Effects on the Levels of Brain Derived Neurotrophic Factor in the Hippocampus and Amygdala
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Recent findings on stress induced structural plasticity in rodents have identified important differences between the hippocampus and amygdala. The same chronic immobilization stress (CIS, 2 h/day) causes growth of dendrites and spines in the basolateral amygdala (BLA), but dendritic atrophy in hippocampal area CA3. CIS induced morphological changes also differ in their temporal longevity--BLA hypertrophy, unlike CA3 atrophy, persists even after 21 days of stress-free recovery. Furthermore, a single session of acute immobilization stress (AIS, 2 h) leads to a significant increase in spine density 10 days, but not 1 day, later in the BLA. However, little is known about the molecular correlates of the differential effects of chronic and acute stress. Because BDNF is known to be a key regulator of dendritic architecture and spines, we investigated if the levels of BDNF expression reflect the divergent effects of stress on the hippocampus and amygdala. CIS reduces BDNF in area CA3, while it increases it in the BLA of male Wistar rats. CIS-induced increase in BDNF expression lasts for at least 21 days after the end of CIS in the BLA. But CIS-induced decrease in area CA3 BDNF levels, reverses to normal levels within the same period. Finally, BDNF is up regulated in the BLA 1 day after AIS and this increase persists even 10 days later. In contrast, AIS fails to elicit any significant change in area CA3 at either time points. Together, these findings demonstrate that both acute and chronic stress trigger opposite effects on BDNF levels in the BLA versus area CA3, and these divergent changes also follow distinct temporal profiles. These results point to a role for BDNF in stress-induced structural plasticity across both hippocampus and amygdala, two brain areas that have also been implicated in the cognitive and affective symptoms of stress-related psychiatric disorders.
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Non-selective activation of BDNF/TrkB signaling in the amygdala leads to maladaptive plasticity resulting in overactivation of this brain region and exacerbated anxiety and fear responses.
“enhanced BDNF/TrkB signaling in the amygdala leads to maladaptive plasticity resulting in overactivation of this brain region and exacerbated anxiety and fear responses (47, 198–200)”
From Psychedelics and Other Psychoplastogens for Treating Mental Illness. (2021) · cites this paper as [200]
The Discussion links elevated BDNF in the basolateral amygdala to increased anxiety and suggests that sustained up-regulation may underlie pathological fear and anxiety after stress. It does not establish that non-selective BDNF/TrkB activation causes amygdala overactivation or these behavioral effects; the Discussion explicitly says the study did not distinguish TrkB from p75NTR signaling. Page numbers were not provided in our copy. (LLM, conf=0.88)
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- Authors
- Lakshminarasimhan, H., & Chattarji, S.
- Affiliations
- Tata Institute of Fundamental Research (IN)
- Corresponding author
- Chattarji, Sumantra
- ORCID
- Chattarji, Sumantra
- Venue
- PLoS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2012-01-17
- Volume
- 7
- Issue
- 1
- Pages
- e30481
- ISSN
- 1932-6203 (ISSN-L)
- PMC
- PMC3260293
- OpenAlex
- W2058006510
- Cited by
- 253
- References
- 42
- Citations by year
- 2026: 11 · 2025: 13 · 2024: 12 · 2023: 15 · 2022: 16 · 2021: 29 · 2020: 19 · 2019: 14 · 2018: 18 · 2017: 23 · 2016: 20 · 2015: 15 · 2014: 24 · 2013: 16 · 2012: 8
- FWCI
- 8.44
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- PLoS ONE (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Wellcome Trust (GR 0701339 MA)
- Directorate for Biological Sciences
- National Centre for Biological Sciences
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Keywords
- brain-derived neurotrophic factor, restraint stress, chronic stress, acute stress, hippocampus, amygdala, basolateral amygdala, CA3, dendritic spine density, dendritic atrophy, structural plasticity, stress recovery, stress-related psychiatric disorders
- MeSH terms
- Amygdala, Animals, Body Weight, Hippocampus, Immunoassay, Male, Restraint, Physical, Stress, Physiological, Stress, Psychological, Time Factors, Rats, Wistar, Brain-Derived Neurotrophic Factor, Rats, CA3 Region, Hippocampal
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