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Cited by 174Treatment of Major DepressionStress Responses and CortisolNeuroscience and Neuropharmacology Research

Molecular mechanisms of neuroplasticity and pharmacological implications: the example of tianeptine

McEwen, Bruce S., Chattarji, Sumantra·2004·European Neuropsychopharmacology
DOI 10.1016/j.euroneuro.2004.09.008
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Abstract

The hippocampal formation, which expresses high levels of adrenal steroid receptors, is a malleable brain structure that is important for certain types of learning and memory. This structure is also vulnerable to the effects of stress hormones which have been reported to be increased in depressed patients, particularly those with severe depression. The amygdala, a structure that plays a critical role in fear learning, is also an important target of anxiety and stress. Certain animal models of depression involve application of repeated stress. Repeated stress promotes behavioral changes that can be associated with these two brain structures such as impairment of hippocampus-dependent memory and enhancement of fear and aggression, which are likely to reflect amygdala function. At a cellular level, opposite responses in the hippocampus and amygdala are observed, namely, shrinkage of dendrites in hippocampus and growth of dendrites in the lateral amygdala, involving in both cases a remodeling of dendrites. Furthermore, stress-induced suppression of neurogenesis has been noted in dentate gyrus. At a molecular level, the effects of repeated stress in the hippocampus involve excitatory amino acids and the induction of the glial form of the glutamate transporter. Chronic treatment with the antidepressant tianeptine may prevent these effects in hippocampus and amygdala.

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  • Chronic stress compromises the ability of an organism to learn, remember, and make decisions, as well as increases levels of anxiety and aggression.

    “Thus, chronic stress compromises the ability of an organism to learn, remember, and make decisions, as well as increases levels of anxiety and aggression.”

    From Sleep Deprivation and Circadian Disruption (2015) · cites this paper as [58]

  • Chronic stress causes atrophy of neurons in the prefrontal cortex and hippocampus, and hypertrophy of neurons in the amygdala.

    “In animal models, chronic stress causes atrophy of neurons in the prefrontal cortex and hippocampus, brain regions involved in executive function, selective attention, and memory. On the other hand, chronic stress leads to hypertrophy of neurons in the amygdala, a region involved in fear, anxiety, and aggression.58”

    From Sleep Deprivation and Circadian Disruption (2015) · cites this paper as [58]

  • Brain regions such as the hippocampus, amygdala, and prefrontal cortex respond to acute and chronic stress by undergoing structural remodeling, which alters behavioral and physiological responses.

    “Brain regions such as the hippocampus, amygdala, and prefrontal cortex respond to acute and chronic stress by undergoing structural remodeling, which alters behavioral and physiological responses.”

    From Protective and damaging effects of stress mediators: central role of the brain (2006) · cites this paper as [21]

  • Allostatic overload resulting from chronic stress in animal models causes atrophy of neurons in the hippocampus and prefrontal cortex and hypertrophy of neurons in the amygdala.

    “Allostatic overload resulting from chronic stress in animal models causes atrophy of neurons in the hippocampus and prefrontal cortex, brain regions involved in memory, selective attention, and executive function, and causes hypertrophy of neurons in the amygdala, a brain region involved in fear and anxiety, as well as aggression.21”

    From Protective and damaging effects of stress mediators: central role of the brain (2006) · cites this paper as [21]

  • The ability to learn and remember and make decisions may be compromised by chronic stress, and may be accompanied by increased levels of anxiety and aggression.

    “Thus, the ability to learn and remember and make decisions may be compromised by chronic stress, and may be accompanied by increased levels of anxiety and aggression.”

    From Protective and damaging effects of stress mediators: central role of the brain (2006) · cites this paper as [21]

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Authors
McEwen, B. S., & Chattarji, S.
Affiliations
  • Rockefeller University (US)
  • Tata Institute of Fundamental Research (IN)
Corresponding author
McEwen, Bruce S.
ORCID
Venue
European Neuropsychopharmacology
Publisher
Elsevier BV
Published
2004-12
Volume
14
Pages
S497-S502
ISSN
0924-977X (ISSN-L)
DOI
10.1016/j.euroneuro.2004.09.008
OpenAlex
W2079853603
Cited by
174
References
60
Citations by year
2026: 2 · 2025: 3 · 2024: 5 · 2023: 7 · 2022: 7 · 2021: 3 · 2020: 2 · 2019: 6 · 2018: 3 · 2017: 6 · 2016: 9 · 2015: 8 · 2014: 7 · 2013: 10 · 2012: 8
FWCI
9.42
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • European Neuropsychopharmacology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
  • Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Keywords
neuroplasticity, tianeptine, hippocampus, amygdala, repeated stress, depression, glucocorticoid receptor, dendritic remodeling, dentate gyrus neurogenesis, excitatory amino acids, glutamate transporters, antidepressants, fear learning, stress hormones
MeSH terms
Animals, Antidepressive Agents, Tricyclic, Depressive Disorder, Humans, Neuronal Plasticity, Thiazepines

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