Cited by 317Neurogenesis and neuroplasticity mechanismsStress Responses and CortisolMemory and Neural Mechanisms

Suppressed proliferation and apoptotic changes in the rat dentate gyrus after acute and chronic stress are reversible

Heine, Vivi M., Maslam, Suharti, Zareno, Jessica, Joëls, Marian, Lucassen, Paul J.·2004·European Journal of Neuroscience

Abstract

Acute stress suppresses new cell birth in the hippocampus in several species. Relatively little is known, however, on how chronic stress affects the turnover, i.e. proliferation and apoptosis, of the rat dentate gyrus (DG) cells, and whether the stress effects are lasting. We investigated how 3 weeks of chronic unpredictable stress would influence the structural dynamic plasticity of the rat DG, and studied newborn cell proliferation, survival, apoptosis, volume and cell number in 10‐week‐old animals. To study lasting effects, another group of animals was allowed to recover for 3 weeks. Based on two independent parameters, bromodeoxyuridine (BrdU) and Ki‐67 immunocytochemistry, our results show that both chronic and acute stress decrease new cell proliferation rate. The reduced proliferation after acute stress normalized within 24 h. Interestingly, chronically stressed animals showed recovery after 3 weeks, albeit with still fewer proliferating cells than controls. Apoptosis, by contrast, increased after acute but decreased after chronic stress. These results demonstrate that, although chronic stress suppresses proliferation and apoptosis, 3 weeks of recovery again normalized most of these alterations. This may have important implications for our understanding of the reversibility of stress‐related hippocampal volume changes, such as occur, for example, in depression.

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Crossref · 10.1046/j.1460-9568.2003.03100.x

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15 of 15 references verified0 citation errors · 0 not checkable

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  • There was no evidence from TUNEL staining that IL-1β and/or acute stress elicit hippocampal cell death either in vitro or in vivo.

    “In the present study, there was no evidence from TUNEL staining that IL-1β and/or acute stress elicit hippocampal cell death either in vitro or in vivo, which is consistent with previous studies (40–42), although there is one report that severe acute stress increases apoptosis (43).”

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Authors
Heine, V. M., Maslam, S., Zareno, J., Joëls, M., & Lucassen, P. J.
Affiliations
University of Amsterdam (NL)
Venue
European Journal of Neuroscience
Publisher
Wiley
Published
2003-12-16
Volume
19
Issue
1
Pages
131-144
ISSN
  • 0953-816X (ISSN-L)
  • 1460-9568
OpenAlex
W2063394935
Cited by
317
References
15
Citations by year
2025: 2 · 2024: 5 · 2023: 7 · 2022: 6 · 2021: 7 · 2020: 7 · 2019: 14 · 2018: 13 · 2017: 14 · 2016: 17 · 2015: 13 · 2014: 20 · 2013: 23 · 2012: 15
FWCI
3.08
Type
journal article
Language
en
Open access
closed
Locations
  • European Journal of Neuroscience (publishedVersion)
  • PubMed (publishedVersion)
  • UvA-DARE (University of Amsterdam) (publishedVersion)
  • Pure Amsterdam UMC (submittedVersion)
  • Data Archiving and Networked Services (DANS) (submittedVersion)
Funders
National Institutes of Health
Topics
  • Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
  • Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
Keywords
chronic stress, acute stress, dentate gyrus, hippocampus, neurogenesis, cell proliferation, apoptosis, stress recovery, structural plasticity, hippocampal volume, depression
MeSH terms
Acute Disease, Animals, Bromodeoxyuridine, Cell Division, Chronic Disease, Male, Nerve Degeneration, Neuronal Plasticity, Stress, Physiological, Rats, Wistar, Apoptosis, Dentate Gyrus, Ki-67 Antigen, Recovery of Function, Rats

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