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Cited by 253Stress Responses and CortisolNerve injury and regenerationMemory and Neural Mechanisms

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Stress Leads to Contrasting Effects on the Levels of Brain Derived Neurotrophic Factor in the Hippocampus and Amygdala

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Lakshminarasimhan, Harini, Chattarji, Sumantra·2012·PLoS ONE
DOI 10.1371/journal.pone.0030481PMC PMC3260293
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Abstract

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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Figure 1 Chronic stress regulates BDNF expression in CA3 and BLA in contrasting manner. Data are presented as mean ± SEM. A Experimental design of chronic stress (CIS+1d) followed by micro dissection of area CA3 from transverse hippocampal sections or BLA from coronal sections. B BDNF expression in area CA3 is decreased after chronic stress (Control, n = 5; CIS+1d, n = 5), C Chronic stress up regulates BDNF expression in BLA (Control, n = 6; CIS+1d, n = 8). Chronic stress induced changes in BDNF expression profile is normalized to respective control level. D Serum corticosterone levels are up regulated after chronic stress in comparison to controls (Control, n = 5; CIS+1d, n = 6). Significant differences *, p<0.05; Unpaired, two-tailed, Student's t-test was used to compare stress and control groups.
Figure 1 Chronic stress regulates BDNF expression in CA3 and BLA in contrasting manner. Data are presented as mean ± SEM. A Experimental design of chronic stress (CIS+1d) followed by micro dissection of area CA3 from transverse hippocampal sections or BLA from coronal sections. B BDNF expression in area CA3 is decreased after chronic stress (Control, n = 5; CIS+1d, n = 5), C Chronic stress up regulates BDNF expression in BLA (Control, n = 6; CIS+1d, n = 8). Chronic stress induced changes in BDNF expression profile is normalized to respective control level. D Serum corticosterone levels are up regulated after chronic stress in comparison to controls (Control, n = 5; CIS+1d, n = 6). Significant differences *, p<0.05; Unpaired, two-tailed, Student's t-test was used to compare stress and control groups.CC BY · PubMed Central
Figure 2 Contrasting profiles of BDNF in CA3 and BLA in response to recovery from chronic stress. Data are presented as mean ± SEM A Experimental design of 21 days of recovery from chronic stress paradigm (CIS+21d). B BDNF expression in area CA3 comes back to control levels post recovery from chronic stress (Control, n = 6; CIS+21d, n = 6), C Chronic stress induced up regulation in BDNF expression in BLA persists even after twenty one days of recovery (Control, n = 4; CIS+21d, n = 6). BDNF expression profile is normalized to respective control level. D The up regulation of serum corticosterone levels persists even after recovery from chronic stress (Control, n = 7; CIS+21d, n = 6). Significant differences *, p<0.05; Unpaired, two-tailed, Student's t-test was used to compare stress and control groups.
Figure 2 Contrasting profiles of BDNF in CA3 and BLA in response to recovery from chronic stress. Data are presented as mean ± SEM A Experimental design of 21 days of recovery from chronic stress paradigm (CIS+21d). B BDNF expression in area CA3 comes back to control levels post recovery from chronic stress (Control, n = 6; CIS+21d, n = 6), C Chronic stress induced up regulation in BDNF expression in BLA persists even after twenty one days of recovery (Control, n = 4; CIS+21d, n = 6). BDNF expression profile is normalized to respective control level. D The up regulation of serum corticosterone levels persists even after recovery from chronic stress (Control, n = 7; CIS+21d, n = 6). Significant differences *, p<0.05; Unpaired, two-tailed, Student's t-test was used to compare stress and control groups.CC BY · PubMed Central
Figure 3 Acute stress modulates BDNF profile differentially in CA3 and BLA. Data are presented as mean ± SEM. A Experimental design of acute stress (AIS+1d) and recovery for 10 days from acute stress (AIS+10d). B BDNF expression in area CA3 in response to acute stress. Acute stress does not change the BDNF levels in CA3 (Control, n = 9; AIS+1d, n = 9; AIS+10d, n = 6, F(2,21) = 2.11, p>0.05). C Acute stress up regulates BDNF expression in BLA and this up regulation persists even after recovery (Control, n = 6; AIS+1d, n = 5; AIS+10d, n = 6, F(2,14) = 4.82, p<0.05). BDNF expression profile was normalized to respective control levels and evaluated by Fisher's post-hoc. D Effect of acute stress and recovery from acute stress on serum corticosterone levels (Control, n = 11; AIS+1d, n = 5; AIS+10d, n = 6, Kruskal-Wallis ANOVA, χ2 (2) = 10.01, p<0.05, Mann-Whitney post-hoc, p<0.05). Significant differences *, p<0.05.
Figure 3 Acute stress modulates BDNF profile differentially in CA3 and BLA. Data are presented as mean ± SEM. A Experimental design of acute stress (AIS+1d) and recovery for 10 days from acute stress (AIS+10d). B BDNF expression in area CA3 in response to acute stress. Acute stress does not change the BDNF levels in CA3 (Control, n = 9; AIS+1d, n = 9; AIS+10d, n = 6, F(2,21) = 2.11, p>0.05). C Acute stress up regulates BDNF expression in BLA and this up regulation persists even after recovery (Control, n = 6; AIS+1d, n = 5; AIS+10d, n = 6, F(2,14) = 4.82, p<0.05). BDNF expression profile was normalized to respective control levels and evaluated by Fisher's post-hoc. D Effect of acute stress and recovery from acute stress on serum corticosterone levels (Control, n = 11; AIS+1d, n = 5; AIS+10d, n = 6, Kruskal-Wallis ANOVA, χ2 (2) = 10.01, p<0.05, Mann-Whitney post-hoc, p<0.05). Significant differences *, p<0.05.CC BY · PubMed Central

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  1. BS McEwen, 1999, Stress and hippocampal plasticity., Annual Review of Neuroscience, 22, 105, 10.1146/annurev.neuro.22.1.105 · DOI · Paper page

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Metadata

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)
DOI
10.1371/journal.pone.0030481
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
Licence
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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